AIR POLLUTION 469

Sulfur dioxide injury is also typified by necrosis, but at much lower levels.A concentration of 0.3 ppm for eight hours is sufficient.3 Lower levels for longerperiods of exposure will produce a diffuse chlorosis (bleaching).

The net result of air pollutant damage goes beyond the apparent superficialdamage to the leaves. A reduction in surface area results in less growth and smallfruit. For commercial crops this results in a direct reduction in income for the farmer.For other plants the net result is likely to be an early death.

Fluoride deposition on plants not only causes them damage but may result in asecond untoward effect. Grazing animals may accumulate an excess of fluoride thatmottles their teeth and ultimately causes them to fallout.

Problems of diagnosis. Various factors make it difficult to diagnose actual air pol-lution damage. Droughts, insects, diseases, herbicide overdoses, and nutrient defi-ciencies all can cause injury that resembles air pollution damage. Also, combinationsof pollutants that alone cause no damage are known to produce acute effects whencombined.4 This effect is known as synergism.

Effects on Health

Susceptible population. It is difficult at best to assess the effects of air pollutionon human health. Personal pollution from smoking results in exposure to air pollut-ant concentrations far higher than the low levels found in the ambient atmosphere.Occupational exposure may also result in pollution doses far above those found out-doors. Tests on rodents and other mammals are difficult to interpret and apply tohuman anatomy. Tests on human subjects are usually restricted to those who wouldbe expected to survive. This leads us to a question of environmental ethics. If the al-lowable concentration levels (standards) are based on results from tests on rodents,they would be rather high. If the allowable concentration levels must also protectthose with existing cardiorespiratory ailments, they should be lower than those re-sulting from the observed effects on rodents.

We noted earlier that the air quality standards were established to protect publichealth with an "adequate margin of safety." In the opinion of the Administrator ofthe EPA, the standards must protect the most sensitive responders. Thus, as you willnote in the following paragraphs, the standards have been set at the lowest level ofobserved effect. This decision has been attacked by some theorists. They say it wouldmake better economic sense to build more hospitals.S However, one also might applythis kind of logic in establishing speed limits for highways, that is, raise the speedlimit and build more hospitals, junk yards, and cemeteries!

Anatomy of the respiratory system. The respiratory system is the primary indica-tor of air pollution effects in humans. The major organs of the respiratory system are

3p. J. O'Gara, "Sulfur Dioxide and Fume Problems and Their Solutions," Industrial Engineering Chem-istry, vol. 14, p. 744, 1922.

41. Hindawi, Air Pollution Injury to Vegetation.

sCharles H. Connolly, Air PolliJrion and Public Health, New York: Holt, Rinehart & Winston, p. 7, 1972.

470 INTRODUCTION TO ENVIRONMENTAL ENGINEERING I

SinusesAd

T

Ph oseE e

Esop

LymphNodes

chusLun

ung

BronchialBronchiole Cilia

I I Mucus FIGURE 6.5A veo us Th . (8 A. e respiratory system. ource: Ir

Pulmonary Pollution Prime/: Copyright 1988 byVein ells National Thberculosis and Respiratory

Diseases Association. Reprinted byCapillaries permission.)

the nose, pharynx, larynx, trachea, bronchi, and lungs (Figure 6-5). The nose, phar-ynx, larynx, and trachea together are called the upper respiratory tract (URT). Theprimary effects of air pollution on the URT are aggravation of the sense of smell andinactivation of the sweeping motion of cilia, which remove mucus and entrapped par-ticles. The lower respiratory tract (LRT) consists of the branching structures knownas bronchi and the lung itself, which is composed of grape-like clusters of sacs calledalveoli. The alveoli are approximately 300 .urn in diameter. The walls of alveoli arelined with capillaries. Carbon dioxide diffuses through the capillary wall into thealveolus, while oxygen diffuses out of the alveolus into the blood cell. The differ-ence in partial pressure of each of the gases causes it to move from the higher tolower partial pressure.

Inhalation and retention of particles. The degree of penetration of particles intothe LRT is primarily a function of the size of the particles and the rate of breathing.Particles greater than 5 to 10 .urn are screened out by the hairs in the nose. Sneezingalso helps the screening process. Particles in the 1 to 2 .urn size range penetrate to thealveoli. These particles are small enough to bypass screening and deposition in theURT, however they are big enough that their terminal settling velocity allows them todeposit where they can do the most damage. Particles that are 0.5 .urn in diameter donot have a large enough terminal settling velocity to be removed efficiently. Smaller

AIR POLLUTION 471

particles diffuse to the alveolar walls. Refer to Figure 6-2 and note that the size of"Lung Damaging Dust" falls in the critical particle size range.

Chronic respiratory disease. Several long-term diseases of the respiratory systemare seriously aggravated by and perhaps may be caused by air pollution. Airwayresistance is the narrowing of air passages because of the presence of irritating sub-stances. The result is that breathing becomes difficult. Bronchial asthma is a formof airway resistance that results from an allergy. An asthma "attack" is the resultof the narrowing of the bronchioles because of a swelling of the mucous membraneand a thickening of the secretions. The bronchioles return to normal after the attack.Chronic bronchitis is currently defined to be present in a person when excess mu-cus in the bronchioles results in a cough for three months a year for two consecutiveyears. Lung infections, tumors, and heart disease must be absent. Pulmonary emphy-sema is characterized by a breakdown of the alveoli. The small grape-like clustersbecome a large nonresilient balloon-like structure. The amount of surface area forgas exchange is reduced drastically. Cancer of the bronchus (lung cancer) is charac-terized by abnormal, disorderly new cell growth originating in the bronchial mucousmembrane. The growth closes off the bronchioles. It is usually fatal.

Carbon monoxide (CO). This colorless, odorless gas is lethal to humans within afew minutes at concentrations exceeding 5,000 ppm. CO reacts with hemoglobin inthe blood to form carboxyhemoglobin (COHb). Hemoglobin has a greater affinityfor CO than it does for oxygen. Thus, the formation of COHb effectively deprivesthe body of oxygen. At COHb levels of 5 to 10 percent, visual perception, manualdexterity, and ability to learn are impaired. A concentration of 50 ppm of CO foreight hours will result in a COHb level of about 7.5 percent. At COHb levels of 2.5to 3 percent, people with heart disease are not able to perform certain exercises aswell as they might in the absence of CORbo A concentration of 20 ppm of CO foreight hours will result in a COHb level of about 2.8 percent.6 (We should note herethat the average concentration of CO inhaled in cigarette smoke is 200 to 400 ppm!)The sensitive populations are those with heart and circulatory ailments, chronic pul-monary disease, developing fetuses, and those with conditions that cause increasedoxygen demand, such as fever.

Hazardous air pollutants (HAPs). Most of the information on the direct humanhealth effects of hazardous air pollutants (also known as air toxics) comes from stud-ies of industrial workers. Exposure to air toxics in the work place is generally muchhigher than in the ambient air. We know relatively little about the specific effects ofthe HAPs at the low levels normally found in ambient air.

The HAPs regulated under the NESHAP program were identified as causalagents for a variety of diseases. For example, asbestos, arsenic, benzene, coke ovenemissions, and radionuclides may cause cancer. Beryllium primarily causes lung

6B. G. Ferris, "Health Effects of Exposure to Low Levels of Regulated Air Pollutants," Journal of theAir Pollution Control Association, vol. 28, pp. 482-497,1978.

472 INTRODUCTION TO ENVIRONMENTAL ENGINEERING I

disease but also affects the liver, spleen, kidneys, and lymph glands. Mercury attacksIthe brain, kidneys, and bowels. Other potential effects from the HAPs are birth de-

fects and damage to the immune and nervous systems.?

Lead (Pb). In contrast to the other major air pollutants, lead is a cumulative poison.A further difference is that it is ingested in food and water, as well as being inhaled.Of that portion taken by ingestion, approximately 5 to 10 percent is absorbed in thebody. Between 20 and 50 percent of the inspired portion is absorbed. Those portionsthat are not absorbed are excreted in the feces and urine. Lead is measured in theurine and blood for diagnostic evidence of lead poisoning.

An early manifestation of acute lead poisoning is a mild anemia (deficiencyof red blood cells). Fatigue, irritability, mild headache, and pallor indistinguishablefrom other causes of anemia occur when the blood level of lead increases to 60 to120 JLg/l00 g of whole blood. Blood levels in excess of 80 JLg/lOO g result in con-stipation and abdominal cramps. When an acute exposure results in blood levelsof lead greater than 120 JLg/I00 g, acute brain damage (encephalopathy) may re-sult.8 Such acute exposure results in convulsions, coma, cardiorespiratory arrest, anddeath. Acute exposures may occur over a period of one to three weeks.

Chronic exposure to lead may result in brain damage characterized by seizures,mental incompetence, and highly active aggressive behavior. Weakness of extensormuscles of the hands and feet and eventual paralysis may also result.

Atmospheric lead occurs as a particulate. The particle size range is between0.16 and 0.43 JLm. Nonsmoking residents of suburban Philadelphia exposed to ap-proximately 1 JLg/m3 of lead in air have blood levels averaging 11 JLg/lOO g. Non-smoking residents of downtown Philadelphia exposed to approximately 2.5 JLg/m3of lead have blood levels averaging 20 JLg/I00 g.9

Nitrogen dioxide (NO2). Exposure to NO2 concentrations above 5 ppm for 15 min-utes results in cough and irritation of the respiratory tract. Continued exposure mayproduce an abnormal accumulation of fluid in the lung (pulmonary edema). The gasis reddish brown in concentrated form and gives a brownish yellow tint at lower con-centrations. At 5 ppm it has a pungent sweetish odor. The average NO2 concentrationin tobacco smoke is approximately 5 ppm. Slight increases in respiratory illness anddecrease in pulmonary function have been associated with concentrations of about0.10 ppm.lO

7 A. S. Kao, "Formation and Removal Reactions of Hazardous Air Pollutants," Journal of the Air andWaste Management Association, 44, pp. 683-696, 1994.8Robert A. Goyer and J. Julian Chilsolm, "Lead," Metallic Contaminants and Human Health, Douglas

H. K. Lee, ed., New York: Academic Press, pp. 57-95, 1972.9U.S. Department of Heallh, Education and Welfare, Survey of Lead in the Atmosphere of Three UrbanCommunities (U.S. Public Heallh Service Publication No. 999-AP-12), Washington, DC: U.S. Govern-ment Printing Office, 1965.loThe discussion on nitrogen dioxide, photochemical oxidants, sulfur oxides, and total suspended par-ticulates follows B. G. Ferris, "Heallh Effects of Exposure to Low Levels of Regulated Air Pollutants,"Journal of the Air Pollution Control Association, pp. 485-491.

AIR POLLUTION 473 I

Photochemical oxidants. Although the photochemical oxidants include peroxy- .

acetyl nitrate (PAN), acrolein, peroxybenzoyl nitrates (PBzN), aldehydes, and nitro-gen oxides, the major oxidant is ozone (03). Ozone is commonly used as an indicatorof the total amount of oxidant present. Oxidant concentrations above 0.1 ppm resultin eye irritation. At a concentration of 0.3 ppm, cough and chest discomfort are in-creased. Those people who suffer from chronic respiratory disease are particularlysusceptible.

PMIO. As noted earlier, large particles are not inhaled deeply into the lungs. Thisis why EPA switched from an air quality standard based on total suspended matterto one based on particles with an aerodynamic diameter less than 10 .urn (PM1o).Studies in the United States, Brazil, and Germany have related higher levels of par-ticulates to increased risk of respiratory, cardiovascular, and cancer-related deaths,as well as pneumonia, lung function loss, hospital admissions, and asthnta.ll

Recent investigations have pointed toward particle sizes smaller than 2.5 .urnas a major contributor to elevated death rates in polluted cities. 12 These epidemiolog-

ical investigations are based on statistical correlations and at this time have not foundwide acceptance in the scientific community. This is primarily because of the lackof a suitable biological mechanism to explain what causes the deaths. Nonetheless,in order to provide an "adequate margin of safety" the EPA Adntinistrator proposeda new standard based on PM2.5 in July 1997.

Sulfur oxides (SOx) and total suspended particulates (TSP). The sulfur oxidesinclude sulfur dioxide (S02), sulfur trioxide (S03), their acids, and the salts of theiracids. Rather than try to separate the effects of S02 and S03, they are usually treatedtogether. There is speculation that a definite synergism exists whereby fine particu-lates carry absorbed S02 to the LRT. The S02 in the absence of particulates wouldbe absorbed in the mucous membranes of the URT.

Patients suffering from chronic bronchitis have shown an increase in respira-tory symptoms when the TSP levels exceeded 350 .ug/m3 and the S02 level wasabove 0.095 ppm. Studies made in Holland at an interval of three years showed thatpulmonary function improved as S02 and TSP levels dropped from 0.10 ppm and230 .ug/m3 to 0.03 ppm and 80 .ug/m3, respectively.

Air pollution episodes. The word episode is used as a refined form of the worddisastel: 13 Indeed, it was the shock of these disasters that stimulated the first modem

legislative action to require control of air pollutants. The characteristics of the threemajor episodes are summarized in Table 6-2. Careful study of the table will revealthat all of the episodes had some things in common. Comparison of these situationsand others where no episode occurred (that is, where the number of dead and ill was

11 T. Reichhardt, "Weighing the Health Risks of Airborne Particulates," Environmental Science and Tech-

nology, 29, pp. 360A-364A, 1995.

12C. A. Pope, et al., American Journal of Respiratory and Critical Care Medicine, 151, pp. 669-674,1995.13In the nuclear power business, they would call it an "incident."

474 INTRODUcrION TO ENVIRONMENTAL ENGINEERING I

TABLE 6-2 IThree major air pollution episodes

Meuse Valley, 1930 Donora, 1948 London, 1952(Oct. 1-5) (Oct. 26-31) (Dec. 5-9)

Population No data 12,300 8,000,000

Weather Anticyclone, Anticyclone, Anticyclone,inversion, and fog inversion, and fog inversion, and fog

Topography River valley River valley River plain

Most probable Industry (including Industry (including Household coal-source of pollutants steel and zinc plants) steel and zinc plants) burning

Nature of the Chemical irritation Chemical irritation Chemical irritationillnesses of exposed of exposed of exposed

membranous membranous membranoussurfaces surfaces surfaces

No. of deaths 63 17 4,000

Time of deaths Began after second Began after second Began on first day ofday of episode day of episode episode

Suspected proximate Sulfur oxides with Sulfur oxides with Sulfur oxides withcause of irritation particulates particulates particulates

(Source: World Health Organization, Air Pollution, 1961, p. 180.)

considerably less) has revealed that four ingredients are essential for an episode. Ifone ingredient is omitted, fewer people will get sick and only a few people can beexpected to die. The crucial ingredients are: (1) a large number of pollution sources,(2) a restricted air volume, (3) failure of officials to recognize that anything is wrong,and (4) the presence of water droplets of the "right" size.14

Although a sufficient quantity of any pollutant is lethal by itself, it is gener-ally agreed that some mix is required to achieve the results seen in these episodes.Atmospheric levels of individual pollutants seldom rise to lethal levels without an ex-plosion or transportation accident. However, the proper combination of two or morepollutants will yield untoward symptoms at much lower levels. The sulfur oxidesand particulates were the most suspect in the three major episodes.

The meteorology must be such that there is little air movement. Thus, the pol-lutants cannot be diluted. Although a valley is most conducive to a stagnation effect,the London episode proved that it isn't necessary. The stagnant conditions must per-sist for several days. Three days appears to be the minimum.

Tragically, each of these hazardous air pollution conditions became lethal be-cause of the failure of city officials to notice anything strange. If they have no mea-

I

surements of pollution levels or reports from hospitals and morgues, city authoritieshave no reason to alert the public, shut down factories, or restrict traffic.

14J. R. Goldsmith, "Effects of Air Pollution on Human Health," Air Pollution, A. C. Stern, ed., NewYork: Academic Press, pp. 554-557,1968.

AIR POLLUTION 475 I

The last and, perhaps, most crucial element is fog.15 The fog droplets must beof the "right" size, namely, in the 1 to 2 .um diameter range or, perhaps, in the rangebelow 0.5 .um. As mentioned earlier, these particle sizes are most likely to penetrateinto the LRT. Pollutants that dissolve into the fog droplet are thus carried deep intothe lung and deposited there.

6-5 ORIGIN AND FATEOF AIR POLLUTANTS

Carbon Monoxide

Incomplete oxidation of carbon results in the production of carbon monoxide. Thenatural anaerobic decomposition of carbonaceous material by soil microorganismsreleases approximately 9 X 1015 moles of methane (C~) to the atmosphere each yearworldwide.16 The natural formation of CO results from an intermediate step in theoxidation of the methane. The hydroxyl radical (OH') serves as the initial oxidizingagent. It combines with C~ to form an alkyl radical: 17

C~ + OH. -+ CH3' + H2O (6-8)

This reaction is followed by a complex series of 39 reactions, which we have over-simplified to the following:

CH3' + 02+ 2(hv) -+ CO + H2 + OH. (6-9)

This says that CH3' and 02 are each zapped by a photon of light energy (hv). Thesymbol v stands for the frequency of the light. The h is Planck's constant = 6.626 X10-34 JIHz.

Anthropogenic sources (those associated with the activities of human beings)include motor vehicles, fossil fuel burning for electricity and heat, industrial pro-cesses, solid waste disposal, and miscellaneous burning of such things as leaves andbrush. Approximately 1 X lW3 moles of CO are released by these sources. Motor

-vehicles account for more than 60 percent of the emission.No significant change in the global atmospheric CO level has been observed

over the past 20 years. Yet the worldwide anthropogenic contribution of combustionsources has doubled over the same time period. Since there is no apparent change inthe atmospheric concentration, a number of mechanisms (sinks) have been proposed

ISThe word "smog" is a term coined by Londoners before World War I to describe the combination ofsmoke and fog that accounted for much of their weather. Los Angeles smog is a misnomer since littlesmoke and no fog is present. In fact, as we shall see later, Los Angeles smog cannot occur without a lot

..of sunshine. "Photochemical smog" is the correct term to describe the Los Angeles haze.

16John H. Seinfeld, Air Pollution, Physical and Chemical Fundamentals, New York, McGraw-Hill,p. 71, 1975.

17S. C. Wofsy, J. C. McConnell, and M. B. McElroy, "Atmospheric C~, CO and CO2," Journal ofGeophysical Research, vol. 67, pp. 4477-4493, 1972.

476 INTRODUCTION TO ENVIRONMENTAL ENGINEERING

to account for the missing CO. The two most probable are

1. Reaction with hydroxyl radicals to form carbon dioxide2. Removal by soil microorganisms

It has been estimated that these two sinks annually consume an amount of CO thatjust equals the production. IS

Hazardous Air Pollutants (HAPs) 1

The EPA has identified 166 categories of major sources and 8 categories of areasources for the HAPs listed in Table 1-5.19 The source categories represent a widerange of industrial groups: fuel combustion, metal processing, petroleum and naturalgas production and refining, surface coating processes, waste treatment and disposalprocesses, agricultural chemicals production, and polymers and resins production.There are also a number of miscellaneous source categories, such as dry cleaningand electroplating.

In addition to these direct emissions, air toxics can result from chemical forma-tion reactions in the atmosphere. These reactions involve chemicals emitted to the at-mosphere that are not listed HAPs and may not be toxic themselves, but can undergoatmospheric transformations to generate HAPs. For organic compounds present inthe gas phase, the most important transformation processes involve photolysis andchemical reactions with ozone, hydroxyl radicals (OH.), and nitrate radicals?OPhotolysis is the chemical fragmentation or rearrangement of a chemical upon theadsorption of radiation of the appropriate wavelength. Photolysis is only importantduring the daytime for those chemicals that absorb strongly within the solar radiationspectrum. Otherwise, reaction with OH. or 03 is likely to predominate. The HAPsmost often formed are formaldehyde and acetaldehyde.

The major removal mechanisms appear to be OH abstraction or addition. Thereaction products lead to the formation of CO and CO2. Eighty-nine of the 189 HAPshave atmospheric lifetimes of less than one day.

Lead

Volcanic activity and airborne soil are the primary natural sources of atmosphericlead. Smelters and refining processes, as well as incineration of lead-containingwastes, are major point sources of lead. Approximately 70 to 80 percent of the leadwhich used to be added to gasoline was discharged to the atmosphere.

18 John H. Seinfe1d, Air Pollution, Physical and Chemical Fundamentals, p. 71.

19Federal Register, "Initial List of Categories of Sources Under Section 1l2(c)(1) of the Clean Air ActAmendments of 1990," Federal Register, 57, p. 31576,1992.20 A. S. Kao, "Formation and Removal Reactions of Hazardous Air Pollutants," Journal of the Air and

Waste Management Association, 44, pp. 683-696, 1994.