Encyclopedia of Environmental Science and Engineering, Volume I and II

AIR POLLUTANT EFFECTS 37

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 com-

munity 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 sus-

ceptibility to pathogens that may result from the destruction

of macrophages and general injury to the lung’s defense

mechanisms.

LEAD

The major source of lead in the air environment has been

motor vehicles; therefore, levels have decreased dramati-

cally as regulations have mandated the elimination of lead

from gasoline because of its health effects and its detrimen-

tal action on the catalytic converters in vehicles. Metal pro-

cessing, 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 cerebel-

lum, and the kidneys, liver, and other organs, and can lead

to osteoporosis and reproductive disorders. Its effects 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, mer-

cury, 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 associ-

ated with exposure to toxic pollutants in the air for a popula-

tion 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 repre-

sent plausible upper bounds that are unlikely to be higher

but could be appreciably lower. The units of unit risk

values are (g/m^3 )^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 aver-

age concentration of the hazardous material in the ambi-

ent 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 g/m^3 , and the unit

risk value of cadmium is 2.3  10 ^3 (g/m^3 )^1 , then the

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

10 2 Asymptomatic

70 10 No appreciable effect, except shortness of breath on vigorous exertion; possible tightness

across the forehead; dilation of cutaneous blood vessels

120 20 Shortness of breath on moderate exertion; occasional headache with throbbing in temples

220 30 Headache; irritable; easily fatigued; judgment disturbed; possible dizziness; dimness of vision

350–520 40–50 Headache; confusion; collapse; fainting on exertion

800–1220 60–70 Unconsciousness; intermittent convulsion; respiratory failure; death if exposure is long

continued

1950 80 Rapidly fatal

Source: Ellenhorn’s Medical Toxicology, 2nd Ed, Baltimore, MD: Lippincott Williams & Wilkins.

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