SUMMARY

Photochemical air pollution or smog is a problem of growing national importance and is attributable largely to the operation of the motor vehicle. Manifestations of this type of air pollution are appearing with increasing frequency and severity in metropolitan areas throughout the United States. Biological studies of animals show that the photochemical reaction products of automotive emissions produce adverse health effects. There is substantial evidence that these effects may appear in humans after extended exposure to air which is known to be polluted with these same products in many of the larger urban areas. Laboratory experiments have demonstrated that reductions of atmospheric hydrocarbons, an important emission from motor vehicles, can reduce photochemical air pollution and such manifestations as eye irritation and plant damage. Other automotive emission such as nitrogen oxides and carbon monoxide have also been determined as significant. Nitrogen oxides, which appear in engine exhaust gases as well as the effluent of other combustion processes, also play an important role in photochemical air pollution. Technical procedures for reducing these emissions are not so clearly established as for hydrocarbons. Carbon monoxide, although not a contributor to atmospheric photochemical reactions, is a directly toxic substance. Technical procedures have been developed with substantially reduce emissions of this pollutant.

Considering the present extent of the automotive air pollution problem and the speed at which it is growing, effective control of these emissions is needed now. The elimination of all automotive effluents might be considered noxious or a nuisance would be desirable. However, technology thus far has not advanced sufficiently to permit the complete control of all sources of automotive emissions.

Ultimate resolution of the problem of automotive air pollution requires further study to improve understanding of the causes and effects of such pollution and the development of more fully effective means of preventing it. In general the needed research is acknowledged to be the responsibility of both industry and Government. The full utilization of available technical personnel is needed to study biological effects, effect of hydrocarbon/oxides-of-nitrogen ratios, reactivity of hydrocarbons, diesel emissions, instrumentations, sampling techniques, analytical methods, and for community air monitoring, and to develop more effective methods of reducing pollutant emissions. Although there is much to learn, control measures should not be delayed pending completion of all the needed research. As new information is developed and appropriate controls become available, the controls should be applied.

In addition to the direct use of devices or other systems for reduction of vehicle pollutant emissions, two supplemental approaches appear to be desirable. First, better means of assuring attention to the maintenance requirements of such devices or systems must be developed. Greater awareness on the part of the vehicle owner and vehicle service personnel of these devices, their importance and maintenance requirements, is essential. Second, increasing the speed of traffic flow in urban areas will reduce overall emissions of exhaust hydrocarbons and carbon monoxide. Therefore, any practicable steps

that can be taken to expedite the movement of traffic will help in pollution control.

Based on the information presented in this report the following conclusions are made:

1. That all necessary steps should be taken to assure the reduction of pollutant emissions from motor vehicles. For this purpose, there is need for (a) further development of emission criteria, and (b) development of means for insuring the national application of currently available technical knowledge for reduction of such emissions.

2. That the need should be recognized for an expanded automotive vehicle air pollution research program to accelerate further development of emission criteria and improve technical capabilities for controls on automotive vehicles.

3. That means be developed through vehicle inspection programs or otherwise to insure appropriate maintenance of vehicle emission control systems.

4. That all practicable measures should be taken to expedite the flow of traffic in urban areas, since this will, in itself, accomplish significant reduction in vehicle pollutant emissions.

THE CURRENT AUTOMOTIVE AIR POLLUTION PROBLEM

INCIDENCE OF PHOTOCHEMICAL SMOG

A growing body of data indicates that photochemical smog occurs in communities throughout the United States. Emission estimates indicate that in large metropolitan communities motor vehicles are responsible for a large percentage of the critical precursors to photochemical smog: about 97 percent of the total olefins, 40 to 80 percent of the total hydrocarbons, and 14 to 67 percent of the oxides of nitrogen.12 It has been shown that the automobile, itself, discharges appreciable quantities of oxides of nitrogen from the exhaust pipe and discharges hydrocarbons from the exhaust pipe, the crankcase, the carburetor, and the fuel tank.3 4 5 6 7 8 9 10

Studies of the composition and the chemical and biological activity of automobile exhaust have indicated a positive relationship between exhaust and smog.11 Correlations of automobile density and driving patterns with atmospheric pollutant concentrations have further linked smog with the automobile. Diurnal variations in oxidant, nitric oxide, and nitrogen dioxide for Washington, D.C., Cincinnati, Philadelphia, Los Angeles, and other large metropolitan areas show similar pollution patterns.12 In these patterns, nitric oxide peaks early in the day during the period of heavy driving, and nitrogen dioxide reaches a peak a little later. Total oxidant peaks at approximately midday; i.e., during the period of maximum heat and solar irradiation.

Documentation of the prevalence and distribution of vehicular pollution throughout the United States is constantly growing. Much of the evidence consists of air quality data on levels of primary vehicular pollutants (hydrocarbons, nitrogen oxide, and carbon monoxide) and on the occurrence of secondary pollutants (ozone or oxidant and nitrogen dioxide) produced through photochemical reactions in the atmos

NOTE. Explanations for footnote references on p. 18.

phere. A number of plant physiologists have documented photochemical smog occurrence by observation of the unique vegetation damage that it causes. 13 14 15 16 17 18 19 20

Total oxidant is a characteristic class of photochemical product in "smog." The concentration of this pollutant is one of the air quality measurements being made continuously in some large metropolitan communities. The adverse level of oxidant associated with odor, eye irritation, plant damage, or reduction in visibility is generally considered to be approximately 0.10 to 0.15 parts per million, potassium iodide method, or about 0.15 to 0.25 parts per million, phenolphthalein method.21

Laboratory investigations show that large reductions in the concentration of hydrocarbons from automobile emissions lower somewhat the ambient oxidant level,22 reduce eye irritation 22 23 and plant damage,22 and inhibit aerosol formation.24 These beneficial effects result not only from the decrease in hydrocarbon concentration but from the reduced ratio of hydrocarbons to nitrogen oxide. The relation between nitrogen dioxide and these photochemical smog effects. is more complex. Oxidant and peroxyacyl nitrate concentrations increase with increasing nitrogen oxide until a level of 0.1 to 0.2 parts per million of nitrogen dioxide is reached. The trend then re

Maximum 1-hour oxidant values equalled or exceeded 0.18 parts per million (potassium iodide) in Cincinnati, Chicago, Washington, DC., New Orleans, and Los Angeles during 1963. During the period January through July 1964, maximum 1-hour oxidant values equaled or exceeded 0.25 parts per million (potassium iodide) in Cincinnati, Philadelphia, St. Louis, Washington, and Los Angeles. The following tabulation summarizes the prevalence of oxidant values at elevated levels in several cities during specified periods from January through

June 1964.

Percent of days having maximum hourly oxidant equal to or greater than

mil

Oxidant concentrations in Washington exceeded 0.10 parts per lion (potassium iodide) on July 1, 2, 7, 16, 17, and 31, 1964. Information on oxidant values from the Cincinnati continuous air monitoring program station for the period July 20 through July 26, 1964, revealed that total oxidant exceeded 0.10 parts per million (potassium iodide) for several hours on each of the 7 days and equaled or exceeded 0.15 parts per million for at least 1 hour on each day except July 22. The hourly average reached a maximum of 0.31 parts per million on July 21.12 Unusually severe plant damage of the photochemical smog type

was observed during this period at the greenhouse of the Robert A. Taft Sanitary Engineering Center in Cincinnati.29

Atmospheric oxidant concentrations equal to or exceeding the generally accepted adverse levels have also been reported in communities shown in the following tabulation:

Two hundred and sixty black mice, of the cancer resistant C-57 strain were exposed to the atmosphere of Los Angeles for a 2-year period.39 Autopsies of these mice revealed that 2 percent had developed pulmonary adenomas (lung tumors). Autopsies of 184 control animals revealed no adenomas.

In another study groups of animals were exposed for 211⁄2 years to Detroit ambient air in a downtown location.40 Control animals were exposed to ambient air filtered through activated charcoal. Preliminary results show that the former group consistently had elevated white blood count and elevated levels of a blood serum enzyme (alkaline phosphatase) as compared with the control group.

Oxidants

Effects on vegetation.-Ozone in concentrations as low as 5 parts per hundred million was observed by Heggestad 142 to cause leaf injury (lesions) to a sensitive strain (Bel W-3) of tobacco plants exposed for 4 hours as measured by the Mast ozone meter.

17

Berry and Ripperton " associated attacks of white pine emergence tipburn with atmospheric oxidant concentrations as low as 6.5 parts per hundred million. Typical injury findings on pine were produced in the greenhouse with ozone concentrations similar to those recorded in the field.

43

Peroxyacyl nitrates in synthesized pure form were found by Darley 13 to produce acute leaf damage symptoms at trace concentrations as low as 0.5 parts per hundred million. The symptoms were characterized by a glazing, bronzing, or silvering of the lower leaf surface of sensitive species, such as petunias.

Effects on animals.-Pulmonary function studies of guinea pigs and mice prior to, during, and after 2-hour exposures to concentrations of ozone as low as 0.34 parts per million revealed increased respiratory rate and decreased tidal volume. Previous exposure to these animals to higher concentrations of ozone did not result in increased tolerance to the gas. Voluntary running activity of the mice was depressed

during exposure to concentrations of ozone between 0.2 and 0.7 parts per million.

Effects on humans.-Young, Shaw, and Bates" exposed 11 healthy subjects (10 males and 1 female) to single 2-hour exposures of 0.6 to 0.8 parts per million ozone. Measurements of pulmonary function were made immediately before and after each experiment and compared to similar tests on the same subjects while breathing clean air. Ozone at this concentration was found to produce a 25-percent reduction in the steady state diffusing capacity of the lung (carbon monoxide method). Values returned to normal after 4 to 6 hours. All subjects but one developed a tracheal irritation and a slight cough lasting for 6 to 12 hours. The exact mechanism of this very significant but transient fall in the diffusing capacity of the lung (loss of significant lung function) is not known at present. The authors suggest that the thickening of the alveolor wall by edema (fluid) as the most likely explanation for it, since these effects are known to result from exposure to higher concentrations of ozone. Hammond 6 in an interim report on morbidity and mortality studies of smokers and nonsmokers in California analyzed the physical complaints of smokers and nonsmokers living in the more and less polluted regions of California in response to a questionnaire. The questionnaire was oriented to the relationship of smoking to health. Cough, loss of appetite, and nausea or vomiting were reported by a somewhat larger percent of men and women in Los Angeles, Riverside, and Orange Counties than by men and women in other, less polluted counties. However, the differences between the two areas were rather small. Shortness of breath, pain, or discomfort in chest, and indigestion were also reported slightly more frequently by subjects in Los Angeles, Riverside, and Orange Counties. Hammond hesitates to draw the conclusion that general air pollution is not of great consequence as a public health problem because of insufficient time to study his subjects over a period of years and other factors cited.

Aldehydes

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Effects on plants. In a recent study, petunias grown in the greenhouse developed necrotic injury in the actively growing foliage which was characteristic of photochemical damage. The injury appeared to be related to the high aldehyde content of the ambient air. The adverse effects developed after 2 days each time the aldehyde concentration exceeded 0.20 parts per million for 2 hours.

Nitrogen dioxide

Effect on animals.-Pulmonary function studies of guinea pigs and mice prior to, during, and after 4-hour exposures to 5.2 parts per million of nitrogen dioxide revealed increased respiratory rate and decreased tidal volume." Voluntary running activity of the mice was depressed during exposures to concentrations of nitrogen dioxide of 7.7 and 20.9 parts per million.

Mice exposed for a 2-hour period to as little as 3.5 parts per million of nitrogen dioxide showed significantly increased susceptibility to respiratory infection when challenged with an aerosol of Klebsiella pneumoniae. This effect was observed up to 27 hours after exposure.

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