National Ambient Air Quality Standards for Nitrogen Dioxide: Proposed Decision

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 50

[AD-FRL-5313-4]

RIN 2060-AC06

National Ambient Air Quality Standards for Nitrogen Dioxide:

Proposed Decision

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed decision.

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SUMMARY: The level for both the existing primary and secondary national

ambient air quality standards (NAAQS) for nitrogen dioxide (NO2)

is 0.053 parts per million (ppm) (100 micrograms per meter cubed

(g/m3)) annual arithmetic average. In accordance with the

provisions of sections 108 and 109 of the Clean Air Act (Act), as

amended, the EPA has conducted a review of the criteria upon which the

existing NAAQS for NO2 are based. The revised

[[Page 52875]]

criteria are being published simultaneously with the issuance of this

proposed decision. After evaluating the revised health and welfare

criteria, under section 109(d)(1) of the Act, the Administrator has

determined that it is not appropriate to propose any revisions to the

primary and secondary NAAQS for NO2 at this time.

DATES: Comments. Written comments on this proposal must be received on

or before January 9, 1996.

Public Hearing. Persons wishing to present oral testimony

pertaining to this proposal should contact EPA at the address below by

October 26, 1995. If anyone contacts EPA requesting to speak at a

public hearing, a separate notice will be published announcing the

date, time, and place where the hearing will be held.

ADDRESSES: Comments on this proposed action should be sent in duplicate

to: U.S. Environmental Protection Agency, Air and Radiation Docket and

Information Center (6102), Room M-1500, 401 M Street, SW, Washington,

DC 20460, ATTN: Docket No. A-93-06. The docket, which contains

materials relevant to this proposed decision, is available for public

inspection and copying (a reasonable fee may be charged) weekdays

between 8:00 a.m. and 5:30 p.m. in the Central Docket Section (CDS) of

EPA, South Conference Center, Room M-1500, telephone (202) 260-7548.

Public Hearing. Persons wishing to present oral testimony

pertaining to this proposal should notify Ms. Chebryll C. Edwards, U.S.

Environmental Protection Agency, Office of Air Quality Planning

Standards, Air Quality Strategies and Standards Division, Health

Effects and Standards Group (MD-15), Research Triangle Park, NC 27711,

telephone number (919) 541-5428.

FOR FURTHER INFORMATION CONTACT: Ms. Chebryll C. Edwards, U.S.

Environmental Protection Agency, Office of Air Quality Planning and

Standards, Air Quality Strategies and Standards Division (MD-15),

Research Triangle Park, NC 27711, telephone (919) 541-5428.

SUPPLEMENTARY INFORMATION: Availability of Related Information. The

revised criteria document, ``Air Quality Criteria for Oxides of

Nitrogen'' (three volumes, EPA-600/8-91/049aF-cF, August 1993: Volume

I, NTIS #PB95124533, $52.00; Volume II, NTIS #PB124525, $77.00; Volume

III, NTIS #PB95124517, $77.00), and the final revised OAQPS Staff

Paper, ``Review of the National Ambient Air Quality Standards for

Nitrogen Oxides: Assessment of Scientific and Technical Information,''

(EPA-452/R-95-005, September 1995) are available from: U.S. Department

of Commerce, National Technical Information Service, 5285 Port Royal

Road, Springfield, Virginia 22161, or call 1-800-553-6847 (a handling

charge will be added to each order). Other documents generated in

connection with this standard review, such as air quality analyses and

relevant scientific literature, are available in the EPA docket

identified above.

The contents of this action are listed in the following outline:

I. Background

A. Legislative Requirements

1. The Standards

2. Related Control Requirements

B. Existing Standards for Nitrogen Dioxide

C. Review of Air Quality Criteria and Standards for Oxides of

Nitrogen

D. Decision Docket

E. Litigation

II. Rationale for Proposed Decision

A. The Primary Standard

1. Basis for the Existing Standard

2. Proposed Decision on the Primary Standard

a. Sensitive Populations Affected

b. Health Effects of Concern

c. Air Quality Considerations

d. Proposed Decision on the Primary Standard

B. The Secondary Standard

1. Direct Effects of Nitrogen Dioxide

a. Vegetation

b. Materials

c. Conclusions Concerning Direct Effects on Vegetation and

Materials

d. Other Related Effects of Nitrogen Dioxide

2. Nitrogen Deposition

a. Terrestrial/Wetland

b. Aquatic

3. Direct Toxic Effects of Ammonia Deposition to Aquatic Systems

4. Proposed Decision on the Secondary Standard

III. Miscellaneous

A. Executive Order 12866

B. Regulatory Flexibility Analysis

C. Impact on Reporting Requirements

D. Unfunded Mandates Reform Act

I. Background

A. Legislative Requirements

1. The Standards

Two sections of the Act govern the establishment and revision of

NAAQS. Section 108 (42 U.S.C. 7408) directs the Administrator to

identify pollutants which ``may reasonably be anticipated to endanger

public health and welfare'' and to issue air quality criteria for them.

These air quality criteria are to ``accurately reflect the latest

scientific knowledge useful in indicating the kind and extent of all

identifiable effects on public health or welfare which may be expected

from the presence of [a] pollutant in the ambient air * * *.''

Section 109 (42 U.S.C. 7409) directs the Administrator to propose

and promulgate ``primary'' and ``secondary'' NAAQS for pollutants

identified under section 108. Section 109(b)(1) defines a primary

standard as one ``the attainment and maintenance of which, in the

judgment of the Administrator, based on the criteria and allowing an

adequate margin of safety, (is) requisite to protect the public

health.'' A secondary standard, as defined in section 109(b)(2), must

``specify a level of air quality the attainment and maintenance of

which, in the judgment of the Administrator, based on (the) criteria,

is requisite to protect the public welfare from any known or

anticipated adverse effects associated with the presence of (the)

pollutant in the ambient air.'' Welfare effects as defined in section

302(h) (42 U.S.C. 7602(h)) include, but are not limited to, ``effects

on soils, water, crops, vegetation, manmade materials, animals,

wildlife, weather, visibility and climate, damage to and deterioration

of property, and hazards to transportation, as well as effects on

economic values and on personal comfort and well-being.''

The U.S. Court of Appeals for the District of Columbia Circuit has

held that the requirement for an adequate margin of safety for primary

standards was intended to address uncertainties associated with

inconclusive scientific and technical information available at the time

of standard setting. It was also intended to provide a reasonable

degree of protection against hazards that research has not yet

identified (Lead Industries Association v. EPA, 647 F.2d 1130, 1154

(D.C. Cir. 1980), cert. denied, 101 S. Ct. 621 (1980); American

Petroleum Institute v. Costle, 665 F.2d 1176, 1177 (D.C. Cir. 1981),

cert. denied, 102 S. Ct. 1737 (1982)). Both kinds of uncertainties are

components of the risk associated with pollution at levels below those

at which human health effects can be said to occur with reasonable

scientific certainty. Thus, by selecting primary standards that provide

an adequate margin of safety, the Administrator is seeking not only to

prevent pollution levels that have been demonstrated to be harmful but

also to prevent lower pollutant levels that may pose an unacceptable

risk of harm, even if the risk is not precisely identified as to nature

or degree.

In selecting a margin of safety, the EPA considers such factors as

the nature and severity of the health effects involved, the size of the

sensitive population(s) at risk, and the kind and degree of the

uncertainties that must be addressed. Given that the ``margin of

safety'' requirement by definition only

[[Page 52876]]

comes into play where no conclusive showing of adverse effects exists,

such factors, which involve unknown or only partially quantified risks,

have their inherent limits as guides to action. The selection of any

numerical value to provide an adequate margin of safety is a policy

choice left specifically to the Administrator's judgment (Lead

Industries Association v. EPA, supra, 647 F.2d at 1161-62).

Section 109(d)(1) of the Act requires that ``not later than

December 31, 1980, and at 5-year intervals thereafter, the

Administrator shall complete a thorough review of the criteria

published under section 108 and the national ambient air quality

standards * * * and shall make such revisions in such criteria and

standards * * * as may be appropriate * * *.'' Section 109(d)(2) (A)

and (B) requires that a scientific review committee be appointed and

provides that the committee ``shall complete a review of the criteria *

* * and the national primary and secondary ambient air quality

standards * * * and shall recommend to the Administrator any * * *

revisions of existing criteria and standards as may be appropriate * *

*.''

The process by which the EPA has reviewed the existing air quality

criteria and standards for NO2 under section 109(d) is described

later in this notice.

2. Related Control Requirements

States are primarily responsible for ensuring attainment and

maintenance of ambient air quality standards. Under title I of the Act

(42 U.S.C. 7410), States are to submit, for EPA approval, State

implementation plans (SIP's) that provide for the attainment and

maintenance of such standards through control programs directed to

sources of the pollutants involved. The States, in conjunction with the

EPA, also administer the prevention of significant deterioration

program (42 U.S.C. 7470-7479) for these pollutants. In addition,

Federal programs provide for nationwide reductions in emissions of

these and other air pollutants through the Federal Motor Vehicle

Control Program under title II of the Act (42 U.S.C. 7521-7574), which

involves controls for automobile, truck, bus, motorcycle, and aircraft

emissions; the new source performance standards under section 111 (42

U.S.C. 7411); and the national emission standards for hazardous air

pollutants under section 112 (42 U.S.C. 7412).

B. Existing Standards for Nitrogen Dioxide

The principal focus of this standard review is the health and

welfare effects associated with exposure to NO2 and other oxides

of nitrogen. Nitrogen dioxide is a brownish, highly reactive gas which

is formed in the ambient air through the oxidation of nitric oxide

(NO). Nitrogen oxides (NOX), the term used to describe the sum of

NO and NO2, play a major role in the formation of ozone in the

atmosphere through a complex series of reactions with volatile organic

compounds. A variety of NOX compounds and their transformation

products occur both naturally and as a result of human activities.

Anthropogenic (i.e., man-made) sources of NOX emissions account

for a large majority of all nitrogen inputs to the environment. The

major sources of anthropogenic NOX emissions are mobile sources

and electric utilities. Ammonia and other nitrogen compounds produced

naturally do play a role in the cycling of nitrogen through the

ecosystem.

At elevated concentrations, NO2 can adversely affect human

health, vegetation, materials, and visibility. Nitrogen oxide compounds

also contribute to increased rates of acidic deposition. Typical peak

annual average ambient concentrations of NO2 range from 0.007 to

0.061 ppm (``Air Quality Criteria for Oxides of Nitrogen,'' (Criteria

Document or CD), U.S. EPA, 1993, p. 7-10). The highest hourly NO2

average concentrations range from 0.04 to 0.54 ppm (CD, 1993, p. 7-10).

Currently, all areas of the U.S., including Los Angeles (which is the

only area to record violations in the last decade), are in attainment

of the annual NO2 NAAQS of 0.053 ppm. The origins, concentrations,

and effects of NO2 are discussed in detail in the ``Review of

National Ambient Air Quality Standards for Nitrogen Dioxide: Assessment

of Scientific and Technical Information,'' (Staff Paper or SP) (SP,

U.S. EPA, 1995) and in the revised Criteria Document (CD, 1993).

On April 30, 1971, under section 109 of the Act, EPA promulgated

identical primary and secondary NAAQS for NO2 at 0.053 ppm annual

average (36 FR 8186). The scientific and medical bases for these

standards are contained in the original criteria document, ``Air

Quality Criteria for Nitrogen Oxides,'' (CD, 1971).

On December 12, 1978 (43 FR 58117), the EPA announced the first

review and update of the 1971 NO2 criteria in accordance with

section 109(d)(1) of the Act as amended. In preparing the Air Quality

Criteria Document, the EPA provided a number of opportunities for

external review and comment. The Clean Air Scientific Advisory

Committee (CASAC) of the EPA Science Advisory Board held meetings in

1979 and 1980 before providing written closure on the revised criteria

document in June 1981 (Friedlander, 1981). This process resulted in the

production of the revised 1982 document, ``Air Quality Criteria for

Oxides of Nitrogen'' (U.S. EPA, 1982a).

A staff paper, which identified critical issues and summarized

staff interpretation of key studies, received verbal closure at a CASAC

meeting in November 1981 and formal written closure in July 1982

(Friedlander, 1982). In the Staff Paper (U.S. EPA, 1982), staff

recommended that the Administrator select an annual standard ``at some

level between 0.05 ppm and 0.08 ppm.'' Based on the analysis of the

criteria, staff concluded that choosing an annual standard within this

range would ``provide a reasonable level of protection against

potential short-term peaks.''

On February 23, 1984, the EPA proposed to retain both the annual

primary and secondary standards at 0.053 ppm annual average and to

defer action on the possible need for a separate short-term primary

standard until further research on health effects of acute exposures to

NO2 could be conducted (49 FR 6866). The CASAC met to consider the

Agency's proposal on July 19-20, 1984. In an October 18, 1984 closure

letter based on weight of evidence, CASAC concurred with the Agency's

recommendation to retain the annual average primary and secondary

standards at 0.053 ppm (Lippmann, 1984). The CASAC further concluded

that, ``while short-term effects from nitrogen dioxide are documented

in the scientific literature, the available information was

insufficient to provide an adequate scientific basis for establishing

any specific short-term standard * * *.'' After taking into account

public comments, the final decision to retain the NAAQS for NO2

was published by EPA in the Federal Register on June 19, 1985 (50 FR

25532).

C. Review of Air Quality Criteria and Standards for Oxides of Nitrogen

On July 22, 1987, in response to requirements of section 109(d) of

the Act, the EPA announced that it was undertaking plans to revise the

1982 Air Quality Criteria Document for Oxides of Nitrogen (52 FR

27580). The EPA held public workshops in July 1990 to evaluate the

scientific data being considered for integration into the CD.

[[Page 52877]]

In November 1991, the EPA released the revised CD for public review and

comment (56 FR 59285).

The revised CD provides a comprehensive assessment of the available

scientific and technical information on health and welfare effects

associated with NO2 and NOX. The CASAC reviewed the CD at a

meeting held on July 1, 1993 and concluded in a closure letter to the

Administrator that the CD ``* * * provides a scientifically balanced

and defensible summary of current knowledge of the effects of this

pollutant and provides an adequate basis for EPA to make a decision as

to the appropriate NAAQS for NO2'' (Wolff, 1993).

In the summer of 1995, the Office of Air Quality Planning and

Standards (OAQPS) finalized the document entitled, ``Review of the

National Ambient Air Quality Standards for Nitrogen Dioxide: Assessment

of Scientific and Technical Information,'' (SP, U.S. EPA, 1995). The

Staff Paper summarizes and integrates the key studies and scientific

evidence contained in the revised CD and identifies the critical

elements to be considered in the review of the NO2 NAAQS.

The Staff Paper received external review at a December 12, 1994

CASAC meeting. The CASAC comments and recommendations were reviewed by

EPA staff and incorporated into the final draft of the Staff Paper as

appropriate. The CASAC reviewed the final draft of the Staff Paper in

June 1995 and responded by written closure letter (see docket A-93-06).

D. Decision Docket

In 1993, the EPA created a docket (Docket No. A-93-06) for this

proposed decision. This docket incorporates by reference a separate

docket established for the criteria document revision (Docket No. ECAO-

CD-86-082).

E. Litigation

On July 21, 1993, the Oregon Natural Resources Council and Jan

Nelson filed suit under section 304 of the Act to compel the EPA to

complete its periodic review of the criteria and standards for NO2

under section 109(d)(1) of the Act (Oregon Natural Resources Council v.

Carol M. Browner, No. 91-6529-HO (D.Or.)). The plaintiffs and the EPA

agreed to a consent decree establishing a schedule for review of the

NO2 NAAQS, which was subsequently modified pursuant to a further

agreement between the parties. The U.S. District Court for the District

of Oregon entered an order on February 8, 1995 requiring the EPA

Administrator to publish a Federal Register notice announcing her

decision on whether or not to propose any modification of the NAAQS for

NO2 by October 2, 1995. The order also requires the Administrator

to sign a notice to be published in the Federal Register announcing the

final decision whether or not to modify the NO2 NAAQS by October

1, 1996.

II. Rationale for Proposed Decision

A. The Primary Standard

1. Basis for the Existing Standard

The current primary NAAQS for NO2 is 0.053 ppm (100

g/m\3\), averaged over 1 year. In selecting the level for the

current standard, the Administrator made judgments regarding the lowest

reported effect levels, sensitive populations, nature and severity of

health effects, and margin of safety. After assessing the evidence, the

Administrator concluded that the annual standard of 0.053 ppm

adequately protected against adverse health effects associated with

long-term exposures and provided some measure of protection against

possible short-term health effects. The June 19, 1985 Federal Register

notice (50 FR 25532) provides a detailed discussion of the bases for

the existing standard.

2. Proposed Decision on the Primary Standard

The Administrator has determined that it is not appropriate to

propose any revisions of the existing NO2 primary standard at this

time. In reaching this proposed decision, the Administrator has

carefully considered the health effects information contained in the

1993 CD, the 1995 Staff Paper, and the advice and recommendations of

the CASAC as presented both in discussion of these documents at public

meetings and in its 1995 closure letter (see docket A-93-06).

The EPA staff identified several factors that the Administrator

should consider in reaching a decision on whether or not to revise the

current primary standard to protect against exposures to NO2.

These factors include: the sensitive populations affected by nitrogen

dioxides, the nature and severity of the health effects, and the

protection afforded by the current standards.

a. Sensitive Populations Affected. Two general groups in the

population may be more susceptible to the effects of NO2 exposure

than other individuals. These groups include persons with pre-existing

respiratory disease and children 5 to 12 years old (SP, 1995, p. 39).

Individuals in these groups appear to be affected by lower levels of

NO2 than individuals in the rest of the population.

Both the 1993 CD and the 1995 Staff Paper support the hypothesis

that those with pre-existing respiratory disease have an enhanced

susceptibility from exposure to NO2. Since these individuals live

with reduced ventilatory reserves, any reductions in pulmonary function

caused by exposure to NO2 have the potential to further compromise

their ventilatory capacity. Compared to healthy individuals with normal

ventilatory reserves who may not notice small reductions in lung

function, those with pre-existing respiratory disease may be prevented

from continuing normal activity following exposure to NO2.

Asthmatic individuals are considered one of the subpopulations most

responsive to NO2 exposure (CD, 1993, p. 16-1). The National

Institutes of Health (1991) estimates that approximately 10 million

asthmatics live in the U.S. Because asthmatics tend to be much more

sensitive to inhaled bronchoconstrictors than nonasthmatics, there is

the added concern that NO2-induced increase in airway response may

exacerbate already existing hyperresponsiveness caused by pre-exposure

to other inhaled materials.

Patients with chronic obstructive pulmonary disease (COPD)

constitute another subpopulation which is more responsive to NO2

exposure than the average population. This group, which is estimated to

be 14 million in the U.S. (U.S. Department of Health and Human

Services, 1990), includes persons with emphysema and chronic

bronchitis. One of the major concerns for COPD patients is that they do

not have an adequate ventilatory reserve and, therefore, would tend to

be more affected by any additional loss of ventilatory function as may

result from exposure to NO2. The available data also indicate that

NO2 might further damage already impaired host defense mechanisms,

thus putting COPD patients at increased risk for lung infection.

Numerous epidemiological studies conducted in homes with gas stoves

provide evidence that children (5-12 years old) are at increased risk

of respiratory symptoms/illness from exposure to elevated NO2

levels (Melia et al., 1977, 1979, 1983; Ekwo et al., 1983; Ware et al.,

1984; Ogston et al., 1985; Dockery et al., 1989a; Neas et al., 1990,

1991, 1992; Dijkstra et al., 1990; Brunekreef et al., 1989; Samet et

al., 1993). Because childhood respiratory illness is very common (Samet

et al., 1983; Samet and Utell, 1990), any impact which NO2 might

have in

[[Page 52878]]

increasing the probability of respiratory illness in children is a

matter of public health concern. This is particularly true in light of

evidence that recurrent childhood respiratory disease may be a risk

factor for later susceptibility to lung damage (Glezen, 1989; Samet et

al., 1983; Gold et al., 1989). In the U.S., there are approximately 35

million children in the age group 5 to 14 years (Centers for Disease

Control, 1990).

b. Health Effects of Concern. Based on the health effects

information contained in the 1993 CD (which evaluates key studies

published through early 1993) and the 1995 Staff Paper, EPA has

concluded that NO2 is the only nitrogen oxide sufficiently

widespread and commonly found in ambient air at high enough

concentrations to be a matter of public health concern. Exposure to

NO2 is associated with a variety of acute and chronic health

effects. The health effects of most concern at ambient or near-ambient

concentrations of NO2 include changes in airway responsiveness and

pulmonary function in individuals with pre-existing respiratory

illnesses and increases in respiratory illnesses in children (5-12

years old).

The changes in airway responsiveness and pulmonary function are

mostly associated with short-term exposures (e.g., less than 3 hours).

Investigations of long-term exposures of animals to NO2 levels

higher than those found in the ambient air provide evidence for

possible underlying mechanisms of NO2-induced respiratory illness

such as those observed in the indoor epidemiological studies described

below. Furthermore, animal studies have also provided evidence of

emphysema caused by long-term exposures to greater than 8 ppm NO2.

The key evidence regarding these effects is summarized below.

(1) Increase in airway responsiveness. There is little, if any,

convincing evidence that healthy individuals experience increases in

airway responsiveness when exposed to NO2 levels below 1.0 ppm.

However, studies of asthmatics have reported some evidence of increased

airway responsiveness caused by short-term exposures (e.g., less than 3

hours) to NO2 at relatively low concentrations (mostly within the

range of 0.2 to 0.3 ppm NO2) which are of concern in the ambient

environment.

Responsiveness of an individual's airways is typically measured by

evaluating changes in airway resistance or spirometry following

challenge with a pharmacologically-active chemical (e.g., histamine,

methacholine, carbachol), which causes constriction of the airways.

Airway hyperresponsiveness is reflected by an abnormal degree of airway

narrowing caused primarily by airway smooth muscle shortening in

response to nonspecific stimuli. Asthmatics experience airway

hyperresponsiveness to certain chemical and physical stimuli and have

been identified as one of the population subgroups which is most

sensitive to short-term NO2 exposure (CD, 1993, p. 16-1).

Several controlled human exposure studies (Ahmed et al., 1983a,b;

Bylin et al., 1985; Hazucha et al., 1982, 1983; Koenig et al., 1985;

Orehek et al., 1981) of asthmatic individuals showed no significant

effect on responsiveness at very low NO2 concentrations of 0.1 to

0.12 ppm. Folinsbee (1992) analyzed data on asthmatics experimentally-

exposed to NO2 in various studies which used challenges producing

increased airway responsiveness in 96 subjects and decreased airway

responsiveness in 73 subjects. For exposures in the range of 0.2 to 0.3

ppm NO2, he found that the excess increase in airway

responsiveness was attributable to subjects exposed to NO2 at

rest. Because NO2 at these levels does not appear to cause airway

inflammation and the increased airway responsiveness appears fully

reversible, implications of the observed increases in responsiveness

remain unclear. It has been hypothesized that increased nonspecific

airway responsiveness caused by NO2 could lead to increased

responses to a specific antigen; however, there is no plausible

evidence to support this.

(2) Decrease in pulmonary function. Nitrogen dioxide induced

pulmonary function changes in asthmatic individuals have been reported

at low, but not high, NO2 concentrations. For the most part, the

small changes in pulmonary function that have been observed in

asthmatic individuals have occurred at concentrations between 0.2 and

0.5 ppm, but not at much higher concentrations (i.e., up to 4 ppm) (CD,

1993, p. 16-3). In one early study of asthmatics, symptoms of

respiratory discomfort were experienced by 4 of 13 asthmatics exposed

to 0.5 ppm for 2 hours; however, Kerr et al. (1979) concluded that the

symptoms were minimal and did not correlate well with functional

changes. In several other studies of asthmatics, very small changes in

spirometry or plethysmography were reported following acute exposures

in the range of 0.1 (Hazucha et al., 1982, 1983) to 0.6 ppm NO2

(Avol et al., 1988). Hazucha found an 8 percent increase in specific

airway resistance (SRaw) after mild asthmatics were exposed to 0.1

ppm NO2 at rest. However, this finding is not considered

statistically significant. Bauer et al., (1986) reported statistically

significant changes in spirometric response in mild asthmatics exposed

for 20 minutes (with mouthpiece) to 0.3 ppm NO2 and cold air. Avol

et al. (1988) found significant changes in SRaw and 1-second forced

expiratory volume (FEV1) as a function of exposure concentration

and duration for all exposure conditions (i.e., exposure of moderately

exercising asthmatics for 2 hours to 0.3 ppm and 0.6 ppm NO2);

however, it was concluded that there was no significant effect of

NO2 exposure on these measures of pulmonary function (CD, 1993, p.

15-47). Exercising adolescent asthmatics exposed (with mouthpiece) to

air, 0.12 ppm and 0.18 ppm NO2, exhibited small changes in

FEV1, but there were no differences in symptoms between air and

either of the NO2 exposures (Koenig et al., 1987a,b). The absence

of spirometry or plethysmography changes in studies (Avol et al., 1986;

Bylin et al., 1985; Linn et al., 1985b; Linn et al., 1986) conducted at

higher NO2 concentrations makes developing a concentration-

response relationship problematic (CD, 1993, p. 15-62). In assessing

the available data on pulmonary function responses to NO2 in

asthmatic individuals, the CD concludes that the most significant

responses to NO2 that have been observed in asthmatics have

occurred at concentrations between 0.2 and 0.5 ppm (CD, 1993, p. 16-3).

Patients with COPD experience pulmonary function changes with brief

exposure to high concentrations (5 to 8 ppm for 5 minutes) or with more

prolonged exposure to lower concentrations (0.3 ppm for 3.75 hours).

(3) Increased occurrence of respiratory illness among children.

Epidemiological evidence includes a meta-analysis of nine

epidemiological studies of children (5-12 years old) living in homes

with gas stoves. The meta-analysis reported that children (ages 5-12

years) living in homes with gas stoves have an increased risk of about

20 percent for developing respiratory symptoms and disease over

children living in homes without gas stoves. This increase in risk

corresponds to each increase of 0.015 ppm NO2 in estimated 2-week

average NO2 exposure, where mean weekly concentrations in bedrooms

reporting NO2 levels were predominantly between 0.008 and 0.065

ppm NO2 (CD, 1993, p. 14-73). A detailed discussion of the studies

included in the meta-analysis can be found in the 1993 CD as well as in

the 1995 Staff Paper.

[[Page 52879]]

In assessing the potential value of the meta-analysis in developing

the basis for a NAAQS for NO2, the Administrator is mindful of the

limitations of the underlying studies. As discussed in the CD and Staff

Paper, the gas stove studies do not provide sufficient exposure

information, including human activity patterns, to establish whether

the observed health effects are related primarily to peak, repeated

peak, or lower, long-term, average exposures to NO2. Furthermore,

both the staff and CASAC concurred that, absent information on exposure

patterns in the gas stove studies, it is not reasonable to extrapolate

the results of these indoor studies to outdoor exposure regimes (SP,

1995). Indoor exposure patterns to NO2 are quite different

compared to outdoor exposure patterns. With potentially much higher

peaks and average indoor exposures than would be found outdoors, it is

extremely difficult to extrapolate the results of the meta-analysis in

a manner which would provide quantitative estimates of health impacts

for outdoor exposures to NO2 (CD, 1993, p. 16-5).

(4) Biological Plausibility. Animal toxicology studies provide

evidence for possible underlying mechanisms of NO2-induced

respiratory illness. These studies have shown that exposure to NO2

can impair components of the respiratory host defense system and

increase susceptibility to respiratory infection. The increased

respiratory symptoms and illness in children reported in the

epidemiology studies cited above may be a reflection of the increased

susceptibility to respiratory infection caused by the impact of

NO2 on pulmonary defenses. Studies that provide a plausible

biological basis for developing such a hypothesis and that highlight

the potential effects associated with long-term exposures to NO2

are discussed in detail in the 1993 CD and 1995 Staff Paper.

Although the pulmonary immune system has not been adequately

studied to assess the impact of NO2 exposure, there is some

indication that NO2 suppresses some systemic immune responses and

that these responses may be both concentration and time dependent. In

the ambient range of exposures, time may be a more important influence

than concentration. However, there were no data showing clearly the

effect of time on effects of long-term, low-level exposures

representing ambient exposure levels.

In the urban air, the typical pattern of NO2 is a low-level

baseline exposure on which peaks are superimposed. When the

relationship of the peak to baseline exposure and of enhanced

susceptibility to bacterial infection was investigated, the results

indicated that no simplistic concentration times time relationship was

present, and that peaks had a major influence on the outcome (Gardner,

1980; Gardner et al., 1982; Graham et al., 1987). Several other animal

infectivity studies (Miller et al. 1987; Gardner et al., 1982; Graham

et al., 1987) offered evidence which indicated that mice exposed to

baseline plus short-term peaks were more susceptible to respiratory

infection than either those exposed to control or background levels of

NO2. This research also indicated that the pattern of NO2

exposure had a major influence on the response.

The weight of evidence provided by animal toxicology supports the

contention that NO2 impairs the ability of host defense mechanisms

to protect against respiratory infection. Although some of the health

endpoints may not be valid for humans (e.g., increased mortality),

there are many shared mechanisms between animals and humans which

support the hypothesis of association between NO2 exposure and

increases in respiratory symptoms and illness reported in the

epidemiological studies.

Based on the information reviewed in the CD and the Staff Paper, it

is clear that at sufficiently high concentrations of NO2 (i.e., >

8 ppm) for long periods of exposure, NO2 can cause morphologic

lung lesions in animals that meet the criteria for a human model of

emphysema (which requires the presence of alveolar wall destruction in

addition to enlargement of the airspace distal to the terminal

bronchiole). Although current information does not permit

identification of the lowest NO2 levels and exposure periods which

might cause emphysema, it is apparent that levels required to induce

emphysematous lung lesions in animals are far higher than any NO2

levels which have been measured in the ambient air.

c. Air Quality Considerations. One of the factors the Administrator

considered in reaching this proposed decision is the relationship

between short-term exceedances of NO2 concentrations and the

annual NO2 mean. In 1994, McCurdy analyzed air quality data from

the period 1988-1992 to determine the estimated number of exceedances

of various NO2 short-term air quality indicators which would occur

given attainment of a range of annual averages. The annual averages

McCurdy analyzed ranged from 0.02 to 0.06 ppm and included the current

NO2 NAAQS of 0.053 ppm. The 1-hour and daily concentration levels

chosen for analyses were 0.15, 0.20, 0.25, and 0.30 ppm. The results of

this analysis are reported in ``Analysis of High 1 Hr NO2 Values

and Associated Annual Averages Using 1988-1992 Data'' (McCurdy, 1994).

In his report, McCurdy concluded that areas attaining the current

annual NO2 NAAQS reported few, if any, 1 hour or daily exceedances

above 0.15 ppm.

Los Angeles is the only city in the U.S. to record violations of

the annual average NO2 NAAQS during the past decade. However, in

1992, Los Angeles reported air quality measurements which meet the

NO2 NAAQS for the first time. Thus, currently, the entire U.S. is

in attainment of the current NO2 NAAQS.

d. Proposed Decision on the Primary Standard. Based on the

assessment of the health and air quality information presented in the

CD and Staff Paper and discussed above, and taking into account the

advice and recommendations of EPA staff and CASAC, the Administrator

has determined pursuant to section 109(d)(1) of the Act, as amended,

that it is not appropriate to propose any revision of the existing

annual primary standard for NO2 at this time.

In reaching this proposed decision, the Administrator took into

account that the existing standard level is well below those levels

associated with chronic effects observed in animal studies. The current

standard also provides substantial protection against those short-term

peak NO2 concentrations at which clinical studies found

statistically-significant changes in pulmonary function or airway

responsiveness. As part of the review of the primary standard, the

Administrator also considered whether a new short-term standard for

NO2 would be appropriate. Based on the available air quality data,

the Administrator concluded that the existing annual standard provides

adequate protection against potential changes in pulmonary function or

airway responsiveness (which most experts would characterize as mild

responses occurring in the range of 0.2 to 0.5 ppm NO2). The

adequacy of the existing annual standard to protect against potential

pulmonary effects is further supported by the absence of documented

effects in some studies at higher (3 to 4 ppm NO2) concentrations

(SP, 1995, p. 43).

In reviewing the scientific bases for an annual standard, the

Administrator finds that the evidence showing the most serious health

effects associated with long-term exposures (e.g., emphysematous-like

alterations in the lung and increased susceptibility to infection)

comes from animal studies conducted at concentrations well above

[[Page 52880]]

those permitted in the ambient air by the current standard. While

recognizing there is no satisfactory method for quantitatively

extrapolating exposure-response results from these animal studies

directly to humans, the Administrator is concerned that there is some

risk to human health from long-term exposure to elevated NO2

levels given the potential seriousness of the effects in animals.

Other evidence suggesting health effects related to long-term, low-

level exposures, such as the epidemiological studies integrated into

the meta-analysis, provides some qualitative support for concluding

that there is a relationship between long-term human exposure to near-

ambient levels of NO2 and adverse health effects. However, the

various limitations in these studies preclude derivation of

quantitative dose-response relationships for the ambient environment.

The Administrator is mindful that there remains substantial uncertainty

about the actual exposures of subjects in the studies that make up the

meta-analysis. The NO2 levels which were monitored in the gas-

stove studies are only estimates of exposure and do not represent

actual exposures. Because the studies collected 2-week average NO2

measurements, one cannot distinguish between relative contributions to

respiratory symptoms and illness of peak, repeated peak and long-term

average exposure to NO2. In addition, indoor exposure patterns to

NO2 are quite different compared to outdoor exposure patterns.

With potentially much higher peaks and average indoor exposures than

would be found outdoors, it is extremely difficult to extrapolate the

results of the meta-analysis in a manner which would provide

quantitative estimates of health impacts for outdoor exposures to

NO2 (CD, 1993, p. 16-5). Given these limitations, the

Administrator concurs with the EPA staff and CASAC that neither the

meta-analysis nor the underlying studies provide a quantitative basis

for standard setting purposes. In her judgement, they do, however,

provide qualitative support for the retention of the existing standard

which provides protection against both peaks and long-term NO2

exposures.

In reaching this proposed decision, the Administrator also took

into account that the available air quality data indicate that if the

existing standard of 0.053 ppm NO2 is attained, the occurrence of

1-hour NO2 values greater than 0.2 ppm would be unlikely in most

areas of the country (McCurdy, 1994). The Administrator also considered

that all areas of the U.S. are in attainment of the current NO2

NAAQS.

After carefully assessing the available health effects and air

quality information, it is the Administrator's judgment that a 0.053

ppm annual standard would keep annual NO2 concentrations

considerably below the long-term levels for which serious chronic

effects have been observed in animals. Retaining the existing standard

would also provide protection against short-term peak NO2

concentrations at the levels associated with mild changes in pulmonary

function and airway responsiveness observed in controlled human

studies. In reaching this judgment, the Administrator fully considered

the 1995 Staff Paper conclusions with respect to the primary standard

and the views of the CASAC (Wolff, 1995). For the above reasons, the

Administrator has determined, under section 109(d)(1) of the Act, as

amended, that it is not appropriate to propose any revision of the

existing primary standard for NO2 of 0.053 ppm annual average at

this time.

B. The Secondary Standard

Nitrogen dioxide and other nitrogen compounds have been associated

with a wide range of effects on public welfare. The effects associated

with nitrogen deposition include acidification and eutrophication of

aquatic systems, potential changes in the composition and competition

of some species of vegetation in wetland and terrestrial systems, and

visibility impairment. The direct effects of NO2 on vegetation and

materials are also considered. The CD and Staff Paper discuss in detail

the major effects categories of concern; the following discussion draws

from these documents.

1. Direct Effects of Nitrogen Dioxides

a. Vegetation. Data evaluated in the 1993 CD indicate that single

exposures to NO2 for less than 24 hours can produce effects on the

growth, development, or reproduction of plants at concentrations that

greatly exceed the ambient levels of NO2 observed in the U.S. In

experiments of 2 weeks or more, with intermittent exposures of several

hours per day, effects on growth or yield start to appear when the

concentration of NO2 reaches the range of 0.1 to 0.5 ppm,

depending on the species of plant and conditions of exposure (CD, 1993,

p. 9-89).

As reported in the 1993 CD (pp. 9-113 to 9-137), several studies

have examined synergistic or additive effects of NO2 and other air

pollutants on plants. These studies report that NO2 in combination

with other pollutants (i.e., sulfur dioxide, ozone) can increase plant

sensitivity, thus lowering concentration and time of exposure required

to produce injury/growth effects. The pollutant concentrations used in

these experimental studies were well above those observed in the

ambient air and at frequency of co-occurrence that are not typically

found in the U.S. (CD, 1993, p. 9-127).

b. Materials. Nitrogen oxides are known to enhance the fading of

dyes; diminish the strength of fabrics, plastics, and rubber products;

assist the corrosion of metals; and reduce the use-life of electronic

components, paints, and masonry. Compared to studies on sulfur oxides,

however, there is only limited information available quantifying the

effects of nitrogen oxides. While NO2 has been qualitatively

associated with materials damage, it is difficult to distinguish a

single causative agent for observed damage to exposed materials because

many agents, together with a number of environmental stresses, act on a

surface throughout its life.

c. Conclusions Concerning Direct Effects on Vegetation and

Materials. Based on the information assessed in the CD and Staff Paper

and taking into account the advice and recommendations of EPA staff and

CASAC, the Administrator has determined that the existing annual

secondary standard appears to be both adequate and necessary to protect

against the direct effects of NO2 on vegetation and materials, and

that it is not appropriate to propose any modifications of the

secondary standard with respect to such effects. In reaching this

proposed decision, the Administrator considered evidence indicating

that attainment of the existing annual secondary standard provides

substantial protection against both long-term and peak NO2

concentrations which may lead to the direct effects described above.

d. Other Related Effects of Nitrogen Dioxide. While NO2 can

contribute to brown haze, the available scientific evidence indicates

that light scattering by particles is generally the primary cause of

degraded visual air quality and that aerosol optical effects alone can

impart a reddish-brown color to a haze layer. Because of this, the

improvement in visual air quality to be gained by reducing NO2

concentrations is highly uncertain at best. In addition, as discussed

in the 1995 Staff Paper, there is no established relationship between

ground level NO2 concentrations at a given point and visibility

impairment due to a plume or regional haze. These considerations led

both the EPA staff

[[Page 52881]]

and CASAC to conclude that establishment of a secondary NO2

standard to protect visibility would not be appropriate. The

Administrator concurs with those judgments.

While concluding that a secondary NO2 standard is not

appropriate to protect visibility, the Administrator is concerned about

visibility impairment in our national parks and wilderness areas. To

address visible plumes that impact the visual quality of Class I areas,

EPA adopted regulations (under section 165(d) of the Act) in 1980. In

addition, EPA is in the process of developing regional haze regulations

under section 169A of the Act.

2. Nitrogen Deposition

As summarized below, the deposition of nitrogen compounds

contributes to a wide range of environmental problems. As discussed in

detail in the 1993 CD and 1995 Staff Paper, nitrogen compounds effect

terrestrial, wetland, and aquatic ecosystems through direct deposition

or by indirectly altering the complex biogeochemical nitrogen cycle. In

assessing the available effects information evaluated in the CD and

Staff Paper, the Administrator is mindful of the scientific complexity

of nitrogen deposition issues and their broad implications for the

environment.

Nitrogen moves through the biosphere via a complex series of

biologically and non-biologically mediated transformations. The

processes that make up the nitrogen cycle and transform nitrogen as it

moves through an ecosystem include: assimilation, nitrification,

denitrification, nitrogen fixation, and mineralization. Similar types

of transformations can be found in diverse habitats, but the organisms

responsible for the transformations and the rates of the

transformations themselves can vary greatly.

Atmospheric deposition of nitrogen can disturb the nitrogen cycle

and result in the acidification of soils, lakes, and streams. It can

also lead to the eutrophication of sensitive estuarine ecosystems by

changing vegetation composition and affecting nutrient balance. Because

a great degree of diversity exists among ecosystem types, as well as in

the mechanisms by which these systems assimilate nitrogen inputs, the

time to nitrogen saturation (i.e., nitrogen input in excess of total

combined plant and microbial nutritional demands) will vary from one

system or site to another. As a consequence, the relationship between

nitrogen deposition rates and their potential environmental impact is

to a large degree site or regionally-specific and may vary considerably

over broader geographical areas or from one system to another because

of the amount, form, and timing of nitrogen deposition, forest type and

status, soil types and status, the character of the receiving

waterbodies, the history of land management and disturbances across the

watersheds and regions, and exposure to other pollutants. Absent better

quantification of these factors, it is difficult to link specific

nitrogen deposition rates with observed environmental effects,

particularly at the national level.

a. Terrestrial/Wetland. The principal effects on soils and

vegetation associated with excess nitrogen inputs include: (1) Soil

acidification and mobilization of aluminum, (2) increase in plant

susceptibility to natural stresses, and (3) modification of inter-plant

competition. Atmospheric deposition of nitrogen can accelerate the

acidification of soils and increase aluminum mobilization if the total

supply of nitrogen to the system (including deposition and internal

supply) exceeds plant and microbial demand. However, the levels of

nitrogen input necessary to produce measurable soil acidification are

quite high. As reported in the Criteria Document (Tamm and Popovic,

1974; Van Miegroet and Cole, 1984), it is estimated that nitrogen

inputs ranging from 50 to 3,900 kilograms per hectare (kg/ha) for 50

and 10 years respectively, would be required to affect a change in soil

potential for hydrogen (pH) of 0.5 pH units. At present, nitrogen

deposition has not been directly associated with the acidification of

soils in the U.S. The potential exists, however, if additions are high

enough for sufficiently long periods of time, particularly in areas

where soils have low buffering capacity. Mobilization of aluminum can

be toxic to plants and, if transported to waterways, can be toxic to

various aquatic species (SP, 1995, pp. 64,65).

Several studies evaluated in the CD and Staff Paper examined the

effects of nitrogen deposition on forest species sensitivity to

drought, cold, or insect attack. While some studies (Margolis and

Waring, 1986; De Temmerman et al., 1988; Waring and Pitman, 1985;

White, 1984) report that increased nitrogen deposition can alter tree

susceptibility to frost damage, insect and disease attack, and plant

community structure, other studies (Klein and Perkins, 1987; Van Dijk

et al., 1990) did not. For example, Margolis and Waring showed that

fertilization of Douglas fir with nitrogen could lengthen the growing

season to the point where frost damage became a problem. However, Klein

and Perkins presented other evidence that showed no additional winter

injury of high elevation conifer forests when fertilized with 40

kilogram total nitrogen/ha/year. On the other hand, De Temmerman et al.

provided data showing increased fungal outbreaks and frost damage on

several pine species exposed to very high ammonia deposition rates (>

350 kg/ha/year). Numbers of species and fruiting bodies of fungi have

also increased concomitantly with nitrogen deposition in Dutch forests

(Van Breeman and Van Dijk, 1988). The CD evaluated a number of other

studies which also gave mixed results as to the impact of excessive

inputs of nitrogen into forest ecosystems (CD, 1993, pp. 10-92,93).

Climate is thought to play a major role in the severe red spruce

decline in the Northeastern U.S., perhaps with some additional

exacerbation due to the direct effects of acid mist on foliage (Johnson

et al., 1992). There is also some evidence that suggests that indirect

effects of nitrogen saturation, namely nitrate and aluminum leaching,

may be contributing factors to red spruce decline in the Southern

Appalachians (CD, 1993, p. 10-74).

In wetland ecosystems, primary biomass production is most commonly

limited by the availability of nitrogen. Several fertilization studies

have reported that nitrogen application can result in changes in

species composition or dominance in wetland systems. Vermeer (1986)

found that in fen and wet grassland communities, grasses tended to

increase in dominance over other species. Jefferies and Perkins (1977)

also found a species-specific change in stem density at a Norfolk,

England, salt marsh after fertilizing monthly with 610 kg NO3

nitrogen/ha/year or 680 kg NH4+ nitrogen/ha/year over a period of

3 to 4 years.

Long-term studies (greater than 3 years) of increased nitrogen

loadings to wetland systems have reported that increases in primary

production can result in changes in species composition and succession

(U.S. EPA, 1993, pp. 10-120-121). Changes in species composition may

occur from increased evapotranspiration (Howes et al., 1986; Logofet

and Alexander, 1984) leading to a changed water regime that favors

different species or from increased nutrient loss from the system

through incorporation into or leaching from aboveground vegetation. In

parts of Europe, historical data seem to implicate pollutant nitrogen

in altering the competitive relationships among plants and threatening

wetland species adapted to habitats of low fertility

[[Page 52882]]

(Tallis, 1964; Ferguson et al., 1984; Lee et al., 1986).

Potential changes in species composition and succession in wetlands

is of particular concern because wetlands are habitats to many rare and

threatened plant species. Some of these plants have adapted to systems

low in nitrogen or with low nutrient levels. For some species, these

conditions can be normal for growth. Therefore, excess nitrogen

deposition can alter these conditions and thus alter species density

and diversity. In the contiguous U.S., wetlands harbor 14 percent (18

species) of the total number of plant species that are formally listed

as endangered. Several species on this list, such as the insectivorous

plants, are widely recognized to be adapted to nitrogen-poor

environments. While changes in species composition and succession are

of concern, such changes have not been associated with nitrogen

deposition in the U.S.

b. Aquatic. Some aquatic systems are potentially at risk from

atmospheric nitrogen additions through the processes of eutrophication

and acidification. Both processes can sufficiently reduce water quality

making it unfit as a habitat for most aquatic organisms and/or human

consumption. Acidification of lakes from nitrogen deposition may also

increase leaching and methylation of mercury in aquatic systems.

Atmospheric nitrogen can enter aquatic systems either as direct

deposition to water surfaces or as nitrogen deposition to the

watershed. In northern climates, nitrate may be temporarily stored in

snow packs and released in a more concentrated form during snow melt.

Nitrogen deposited to the watershed is then routed (e.g., through plant

biomass and soil microorganisms) and transformed (e.g., into other

inorganic or organic nitrogen species) by watershed processes, and may

eventually run off into aquatic systems in forms that are only

indirectly related to the original deposition. The contributions of

direct and indirect atmospheric loadings have received increased

attention. While the available evidence indicates that the impact of

nitrogen deposition on sensitive aquatic systems can be significant, it

is difficult to quantify the relationship between atmospheric

deposition of nitrogen, its appearance in receiving waters, and

observed effects.

(1) Acidification. In the U.S., the most comprehensive assessment

of chronic acidification of lakes and streams comes from the National

Surface Water Survey (NSWS) conducted as part of the National Acid

Precipitation Assessment Program (NAPAP). A detailed discussion of the

findings in the NSWS can be found in both the 1993 CD and the 1995

Staff Paper. The studies highlighted in these documents reported mixed

observations as to the relative contribution of nitrogen compounds to

chronic acidification in North American lakes. However, the National

Stream Survey (NSS) data do suggest that the Catskills, Northern

Appalachians, Valley and Ridge Province, and Southern Appalachians all

show some potential for chronic acidification due to nitrate ions

(NO3). Two studies (Kaufmann et al., 1991; Driscoll et al., 1989)

have examined whether atmospheric deposition is the source of the

NO3 leaking out of these watersheds. Data from the NSS (Kaufmann

et al., 1991) suggest a strong correlation between concentrations of

stream water and levels of wet nitrogen deposition in each of the NSS

regions. Secondly, Driscoll et al. (1989) collected input/output budget

data for a large number of watersheds in the U.S. and Canada and

summarized the relationship between nitrogen export and nitrogen

deposition at all the sites. Though the relationships discovered should

not be over-interpreted or construed as an illustration of cause and

effect, they do show that watersheds in many regions of North America

are retaining less than 75 percent of the nitrogen that enters them,

and that the amount of nitrogen being leaked from these watersheds is

higher in areas where nitrogen deposition is highest.

On a chronic basis in the U.S., especially in the eastern part of

the country, nitrogen deposition does play a role in surface water

acidification. However, there are significant uncertainties with regard

to the long-term role of nitrogen deposition in surface water acidity

and with regard to the quantification of the magnitude and timing of

the relationship between atmospheric deposition and the appearance of

nitrogen in surface waters.

Episodic acidification in surface waters is a concern in the

Northeast, Mid-Atlantic, Mid-Atlantic Coastal Plain, Southeast, Upper

Midwest, and West regions (Wigington et al., 1990). In the Mid-Atlantic

Coastal Plain and Southeast regions, all of the episodes reported to

date have been associated with rainfall. In contrast, most of the

episodes in the other regions are related to snowmelt, although rain-

driven episodes apparently can occur in all regions of the country. It

is important to stress that even within a given area, such as the

Northeast, major differences can be evident in the occurrence, nature,

location (lakes or streams), and timing of episodes at different sites.

The 1995 Staff Paper provides a detailed description of the processes

which may contribute to the timing and severity of acidic episodes.

Some broad geographic patterns in the frequency of episodes in the

U.S. are now evident. Episodes driven by NO3 are common in the

Adirondacks and Catskill Mountains of New York, especially during

snowmelt, and also occur in at least some streams in other portions of

the Northeast (e.g., Hubbard Brook). Nitrate contributes on a smaller

scale to episodes in Ontario and may play some role in episodic

acidification in the Western U.S. There is little current evidence that

NO3 episodes are important in the acid-sensitive portions of the

Southeastern U.S. outside the Great Smoky Mountains. There is no

information on the relative contribution of NO3 to episodes in

many of the subregions covered by the NSS, including those that

exhibited elevated NO3 concentrations at spring base flow (e.g.,

the Appalachian Plateau, the Valley and Ridge Province and Mid-Atlantic

Coastal Plain), because temporally-intensive studies have not been

published for these areas.

While the available data suggest that NO3 episodes are more

severe now than they were in the past, it is important to emphasize

that only the data reported for the Catskills can be considered truly

long-term (up to 65 years of record). Data for the Adirondacks

(Driscoll and Van Dreason, 1993) and other areas of the U.S. (Smith et

al., 1987) span only 1 to 2 decades and should be interpreted with

caution.

Because surface water nitrogen increases have occurred at a time

when nitrogen deposition has been relatively unchanged in the

Northeastern U.S. (Husar, 1986; Simpson and Olsen, 1990), it is

suggestive that nitrogen saturation of watersheds is progressing and

that current levels of nitrogen deposition are too high for the long-

term stability of aquatic systems in the Adirondacks, the Catskills,

and possibly elsewhere in the Northeast. It is important to note that

this supposition is dependent on our acceptance of NO3 episodes as

evidence of nitrogen saturation. While there is some support for this,

there are significant uncertainties with respect to the quantification

of the linkage and the timing of the relationship between the

atmospheric deposition of nitrogen and its episodic or chronic

appearance in surface waters.

This relationship between deposition and effect becomes more

complex because the capacity to retain nitrogen

[[Page 52883]]

differs from one watershed to another and from one region to another as

watershed and regional features differ. The differing features that may

contribute to these differences include, the amount, form and timing of

nitrogen deposition, forest type and status (including soil type and

status), the character of the receiving waterbodies, the history of

land management and disturbances across watersheds and regions and

exposure to other pollutants. For example, the Northeast, because of

the presence of aggrading forests and deeper soils in comparison to

those of the West, may be able to absorb higher rates of deposition

without serious effects than areas of the mountainous West, where soils

are thin in comparison and forests are often absent at the highest

elevations (CD, p. 10-179). The data of Silsbee and Larson (1982)

suggest strongly that forest maturation is also linked to the process

of NO3 leakage from Great Smoky Mountain watersheds.

In summary, the available data indicate that nitrogen contributes

to episodic acidification of sensitive streams and lakes in the

Northeast. The data also suggest that some watersheds of the Northeast

and the mid-Appalachians may be nearing nitrogen saturation. If, and

when, this occurs, nitrogen deposition will become a more direct cause

of chronic surface water acidification. At present, however, it is

difficult to establish quantitative relationships between nitrogen

deposition and the appearance of nitrogen in receiving waters, given

the uncertainties in determining time to nitrogen saturation for

varying systems and sites. The complexity of the scientific issues

involved led the CASAC to conclude that available scientific

information assessed in the Criteria Document and Staff Paper did not

provide an adequate basis for standard setting purposes at this time

(see Wolff, 1995). In its review of the Acid Deposition Standard

Feasibility Study: Report to Congress (U.S. EPA, 1995), the Acid

Deposition Effects Subcommittee of the Ecological Processes and Effects

Committee of the EPA's Science Advisory Board also concluded that there

was not an adequate scientific basis for establishing an acidic

deposition standard (see ``An SAB Report: Review of the Acid Deposition

Standard Feasibility Study Report to Congress,'' U.S. EPA, 1995).

(2) Eutrophication. Eutrophication is the process by which aquatic

systems are enriched with the nutrient(s) that are presently limiting

for primary production in that system. Eutrophication may produce

conditions of increased algal biomass and productivity, nuisance algal

populations, and decreases in oxygen availability for heterotrophic

organisms. Another effect of chronic eutrophication is increased algal

biomass shading out ecologically-valuable estuarine seagrass beds.

Eutrophy can lead to fish kills and the permanent loss of some

sensitive species caused by suffocation or rarely because of some kind

of toxic algal bloom. Though this process often occurs naturally over

the long-term evolution of lakes, it can be significantly accelerated

by the additional input of the limiting nutrients from anthropogenic

sources. In order to establish a link between nitrogen deposition and

the eutrophication of aquatic systems, one must first demonstrate that

the increase in biomass within the system is limited by nitrogen

availability, and second, that nitrogen deposition is a major source of

nitrogen to the system.

In most freshwater systems, phosphorus, not nitrogen, is the

limiting nutrient. Therefore, eutrophication by nitrogen inputs will

only be a concern in lakes that are chronically nitrogen limited and

have a substantial total phosphorous concentration. This condition is

common only in lakes that have received excessive inputs of

anthropogenic phosphorous, or in rare cases, have high concentrations

of natural phosphorus. In the former case, the primary dysfunction of

the lakes is an excess supply of phosphorous, and controlling nitrogen

deposition would be an ineffective method of gaining water quality

improvement. In the latter case, lakes with substantial total

phosphorous concentrations would experience measurable increases in

biomass from increases in nitrogen deposition.

In contrast to freshwater systems, the productivity of estuarine

waters of the U.S. correlates more closely with supply rates of

nitrogen than of other nutrients (Nixon and Pilson, 1983). Because

estuaries and coastal waters receive substantial amounts of weathered

material from terrestrial ecosystems and from exchange with sea water,

acidification is not a concern. However, this same load of weathered

material and anthropogenic inputs makes these same areas prone to the

effects of eutrophication.

Considerable research has focused on whether estuarine and coastal

ecosystems are limited by nitrogen, phosphorus, or some other factor.

Numerous geochemical and experimental studies have suggested that

nitrogen limitation is much more common in estuarine and coastal waters

than in freshwater systems (CD, 1993, pp. 10-189 to 197). However,

specific instances of phosphorus limitation (Smith, 1984) and of

seasonal switching between nitrogen and phosphorus limitation (D'Elia

et al., 1986; McComb et al., 1981) have been observed.

Estimation of the contribution of nitrogen deposition to the

eutrophication of estuarine and coastal waters is made difficult by the

multiple direct anthropogenic sources (e.g., from agriculture and

sewage) of nitrogen. In the U.S., only a few systems have been studied

with enough intensity to develop predictions about the contribution of

atmospheric nitrogen to total nitrogen inputs. One example is the

Chesapeake Bay, where a large effort has been made to establish the

relative importance of different sources of nitrogen to the total

nitrogen load entering the bay (e.g., D'Elia et al., 1982; Smullen et

al., 1982; Fisher et al., 1988a; Tyler, 1988). The signatories to the

Chesapeake Bay Agreement (i.e., Maryland, Virginia, Pennsylvania, the

District of Columbia, and EPA, through their Baywide Nutrient Reduction

Strategy and individual tributary watershed nutrient reduction

strategies) have committed to reduce nitrogen and phosphorus loadings

to the bay by 40 percent (from 1985 baseline) by the year 2000.

Enhanced modeling is being used to better assess source

responsibility for the transport and deposition of nitrogen from the

350,000 square miles Chesapeake Bay airshed. This enhanced modeling

will assist EPA in deciding: (1) Whether to include reductions in

atmospheric NOX and resultant decreased loadings via atmospheric

deposition in the reductions of total nitrogen loading necessary to

achieve the planned 40 percent reduction goal by the year 2000, and (2)

the role implementation of the Act will play in ensuring nitrogen

loadings are capped at the 40 percent reduction goal beyond the year

2000 in the face of significant projected population increases within

the Chesapeake Bay watershed (and surrounding airshed). This

integration of modeling, watershed, and airshed management will serve

as a case study and a prototype method for other geographic areas.

Though estimates for each individual source are very uncertain,

studies undertaken to determine the proportion of the total NO3

load to the bay, which was attributable to nitrogen deposition,

produced estimates in the range of 18 to 39 percent. These estimates,

which reflect the current status of the area, suggest that supplies of

nitrogen from deposition exceed supplies from all

[[Page 52884]]

other non-point sources (i.e., farm runoff) to the bay and only point-

source inputs (i.e., discharges to water, emissions from industrial

facilities) represent a greater input than deposition.

Based on the available data, it is clear that atmospheric nitrogen

inputs to estuarine and coastal ecosystems are of concern. The

importance of atmospheric inputs will vary, however, from site to site

and will depend on the availability of other growth nutrients, the

flushing rate through the system, the sensitivity of resident species

to added nitrogen, the types and chemical forms of nitrogen inputs from

other sources, as well as other factors. Given these complexities,

site-specific investigations, such as the Chesapeake Bay Study, are

needed to ascertain the most effective mitigation strategy. Similar

place-based studies are already under way in the Tampa Bay and other

coastal areas.

3. Direct Toxic Effects of Ammonia Deposition to Aquatic Systems

Nitrogen deposition could potentially contribute directly to toxic

effects in surface waters. High ammonia concentrations are associated

with lesions in gill tissue, reduced growth rates of trout fry, reduced

fecundity (number of eggs), increased egg mortality, and increased

susceptibility of fish to other diseases, as well as a variety of

pathological effects in invertebrates and aquatic plants. Given current

maximal concentrations of ammonium ions (NH4+) in wet deposition

and reasonable maximum rates of dry deposition, even if all nitrogen

species were ammonified, the maximum potential NH4+ concentrations

attributable to deposition would be approximately 280 nmol/L and would

be unlikely to be toxic except in unusual circumstances. Therefore, it

appears that the potential for toxic effects directly attributable to

nitrogen deposition in the U.S. is very limited. In addition, EPA has

established water quality standards for ammonia to protect against

these effects (50 FR 30784, July 29, 1984; also see guidance document

EPA-440/5-85-001).

4. Proposed Decision on the Secondary Standard

As discussed above, after carefully considering the information on

the direct effects of NO2, the Administrator has determined that

the existing annual secondary standard is both necessary and adequate

to protect vegetation and materials from the direct effects of

NO2. The Administrator has also determined that establishment of a

secondary NO2 standard to protect visibility is not appropriate.

In reaching these provisional conclusions, the Administrator has

assessed the evidence provided in the CD and the Staff Paper as well as

the advice and recommendations of the EPA staff and CASAC.

With respect to nitrogen deposition, the Administrator is concerned

about the growing body of scientific information, assessed in the CD

and Staff Paper and discussed above, that associates nitrogen

deposition with a wide range of environmental effects. Of particular

concern is the available data that indicate nitrogen deposition plays a

significant role in the episodic acidification of certain sensitive

streams and lakes and could cause long-term chronic acidification of

such surface waters. The Administrator notes, as did CASAC, that

because of the variations in the actual rate of nitrogen uptake,

immobilization, denitrification, and leaching, it is very difficult,

given current quantification of these processes, to link specific

nitrogen deposition rates with observed environmental effects.

In considering the available data, the Administrator is also

mindful, given the complex processes involved, that the time to

nitrogen saturation will vary from one system to another. As a

consequence, the relationship between nitrogen deposition rates and

their potential environmental impact is to a large degree site- or

regionally-specific and may vary considerably over broader geographical

areas. These complexities led both the EPA and CASAC to conclude that

there is currently insufficient information to set a national secondary

NO2 standard which would protect against the acidification effects

of nitrogen deposition. Because of the site- and regional-specific

nature of the problem, the staff also questioned whether adoption of a

national secondary NO2 standard would be an effective tool to

address such effects.

In considering the staff's latter view, the Administrator also

recognizes that Congress reserved judgment regarding the possible need

for further action to control acid deposition beyond the provisions of

title IV of the 1990 Amendments and what form any such action might

take (Pub. L. 101-549, sec. 404, 104 Stat. 2399, 2632 (1990)). For a

more complete discussion of the congressional deliberation on the

acidic deposition issue, see 58 FR 21356-21357, April 21, 1993. Among

other things, Congress directed EPA to conduct a study of the

feasibility and effectiveness of an acid deposition standard(s), to

report to Congress on the role that a deposition standard(s) might play

in supplementing the acidic deposition program adopted in title IV, and

to determine what measures would be needed to integrate it with that

program. The resulting document entitled, ``Acid Deposition Standard

Feasibility Study: Report to Congress'' (U.S. EPA, 1995), concluded, as

did the CD and staff paper, that nitrogen deposition plays a

significant role in the acidification of certain sensitive streams and

lakes and that the time to nitrogen saturation varies significantly

from one system or region to another. The complexities of watershed

nitrogen dynamics (e.g., the biological processes) and the

uncertainties in modeling results that project future effects of

nitrogen deposition under alternative emission scenarios, however, led

EPA staff (as well as the Acid Deposition Effects Subcommittee of the

Ecological Processes and Effects Committee of the EPA's Science

Advisory Board that reviewed the report) to conclude that current

scientific uncertainties associated with determining the level(s) of an

acid deposition standard(s) are significant (see ``An SAB Report:

Review of the Acid Deposition Standard Feasibility Study Report to

Congress,'' U.S. EPA, 1995). The study does not advocate setting an

acid deposition standard at this time. The study does, however, set

forth a range of regionally-specific goals to help guide the policy

maker when assessing NOX control strategies and their potential

for reducing nitrogen deposition effects.

The Administrator has also examined the available information that

indicates atmospheric nitrogen deposition can play a significant role

in the eutrophication of estuarine and coastal waters. However,

estimation of the contribution of nitrogen deposition to the

eutrophication of estuarine and coastal waters is made difficult by

multiple direct anthropogenic sources of nitrogen. Thus, the importance

of atmospheric inputs will vary from site to site and will depend on

the availability of other growth nutrients, the flushing rate through

the system, the sensitivity of resident plant species to added

nitrogen, as well as the types of chemical forms of nitrogen inputs

from other sources. Given the complexities of these factors and the

limited data currently available, the Administrator concurs with the

EPA staff and CASAC conclusion that there is not sufficient

quantitative information to establish a national secondary standard to

protect sensitive ecosystems from the eutrophication effects caused by

[[Page 52885]]

nitrogen deposition. Rather, additional site-specific investigations

(such as the Chesapeake Bay Study) are needed to ascertain the most

effective mitigation strategies.

For the above reasons, the Administrator has determined pursuant to

section 109(d)(1) of the Act, as amended, that it is not appropriate to

propose any revision of the current secondary standard for NO2 to

protect against welfare effects at this time. As provided for under the

Act, the EPA will continue to assess the scientific information on

nitrogen-related effects as it emerges from ongoing research and will

update the air quality criteria accordingly. These revised criteria

should provide a more informed basis for reaching a decision on whether

a revised NAAQS or other regulatory measures are needed in the future.

In the interim, the 1990 Clean Air Act Amendments (Pub. L. 101-549,

104 Stat. 2399 (1990)) require EPA to promulgate a number of control

measures to reduce NOX emissions from both mobile and stationary

sources. These reductions are in addition to those required under title

IV of the 1990 Amendments (Pub. L. 101-549, secs. 401-413, 104 Stat.

2399, 2584-2634 (1990)). Title IV, in conjunction with other titles of

the Act, requires EPA to reduce nitrogen oxide emissions by

approximately two million tons from 1980 emission levels. The

reductions achieved through these EPA initiatives will provide

additional protection against the potential acute and chronic effects

associated with exposure to NOX while EPA continues to generate

and review additional information on the effects of oxides of nitrogen

on public welfare and the environment. The EPA believes it is important

to continue to recognize the benefit to the environment that can be

achieved by further reducing NOX emissions. Therefore, as part of

this process, the EPA will integrate, to the extent appropriate,

nitrogen deposition considerations when assessing new NOX control

strategies.

III. Miscellaneous

A. Executive Order 12866

Under Executive Order 12866, the Agency must determine whether a

regulatory action is ``significant'' and, therefore, subject to Office

of Management and Budget (OMB) review and the requirements of the

Executive Order. The order defines ``significant regulatory action'' as

one that may:

(1) Have an annual effect on the economy of $100 million or more or

adversely affect in a material way the economy, a sector of the

economy, productivity, competition, jobs, the environment, public

health or safety, or State, local, or tribal governments or

communities;

(2) create a serious inconsistency or otherwise interfere with an

action taken or planned by another Agency;

(3) materially alter the budgetary impact of entitlements, grants,

user fees, or loan programs or the rights and obligations or recipients

thereof; or

(4) raise novel legal or policy issues arising out of legal

mandates, the President's priorities, or the principles set forth in

the Executive Order.

Although the EPA is not proposing any modification of the existing

NO2 NAAQS, the OMB has advised the EPA that this proposal should

be construed as a ``significant regulatory action'' within the meaning

of the Executive Order. Accordingly, this action was submitted to the

OMB for review. Any changes made in response to OMB suggestions or

recommendations will be documented in the public record.

B. Regulatory Flexibility Analysis

The Regulatory Flexibility Act (RFA) requires that all Federal

agencies consider the impacts of final regulations on small entities,

which are defined to be small businesses, small organizations, and

small governmental jurisdictions (5 U.S.C. 601 et seq.). These

requirements are inapplicable to rules or other administrative actions

for which the EPA is not required by the Administrative Procedure Act

(APA), 5 U.S.C. 551 et seq., or other law to publish a notice of

proposed rulemaking (5 U.S.C. 603(a), 604(a)). The EPA has elected to

use notice and comment procedures in deciding whether to revise the

NO2 standards based on its assessment of the importance of the

issues. Under section 307(d) of the Act, as the EPA interprets it,

neither the APA nor the Act requires rulemaking procedures where the

Agency decides to retain existing NAAQS without change. Accordingly,

the EPA has determined that the impact assessment requirements of the

RFA are inapplicable to the decision proposed in this notice.

C. Impact on Reporting Requirements

There are no reporting requirements directly associated with an

ambient air quality standard promulgated under section 109 of the Act

(42 U.S.C. 7400). There are, however, reporting requirements associated

with related sections of the Act, particularly sections 107, 110, 160,

and 317 (42 U.S.C. 7407, 7410, 7460, and 7617). This proposal will not

result in any changes in these reporting requirements since it would

retain the existing level and averaging times for both the primary and

secondary standards.

D. Unfunded Mandates Reform Act

Title II of the Unfunded Mandates Reform Act of 1995 (UMRA), P.L.

104-4, establishes requirements for Federal agencies to assess the

effects of their regulatory actions on State, local, and tribal

governments and the private sector. Under section 202 of the UMRA, EPA

generally must prepare a written statement, including a cost-benefit

analysis, for proposed and final rules with ``Federal mandates'' that

may result in expenditures to State, local and tribal governments, in

the aggregate, or to the private sector, of $100 million or more in any

1 year. Before promulgating an EPA rule for which a written statement

is needed, section 205 of the UMRA generally requires EPA to identify

and consider a reasonable number of regulatory alternatives and adopt

the least costly, most cost-effective or least burdensome alternative

that achieves the objectives of the rule. The provisions of section 205

do not apply when they are inconsistent with applicable law.

Before EPA establishes any regulatory requirements that may

significantly or uniquely affect small governments, including tribal

governments, it must have developed, under section 203 of the UMRA, a

small government agency plan. The plan must provide for notifying

potentially affected small governments, enabling officials of affected

small governments to have meaningful and significant Federal

intergovernmental mandates, and informing, educating, and advising

small governments on compliance with the regulatory requirements.

A decision by the Administrator pursuant to section 109(d) of the

Act not to propose any revision of the existing national primary and

secondary standards for NO2 does not require rulemaking

procedures, and EPA has elected to provide notice and an opportunity

for comment concerning this proposed decision in view of the importance

of the issues. If the Administrator makes a final decision not to

modify the existing NAAQS for NO2, this will not impose any new

expenditures on governments or on the private sector, or establish any

new regulatory requirements affecting small governments. Accordingly,

the EPA has determined that the provisions of sections 202, 203, and

205 of the UMRA do not apply to this proposed decision.

List of Subjects in 40 CFR Part 50

Environmental protection, Air pollution control, Carbon monoxide,

[[Page 52886]]

Lead, Nitrogen dioxide, Ozone, Particulate matter, Sulfur oxides.

Dated: October 2, 1995.

Carol M. Browner,

Administrator.

References

(1) Ahmed, T.; Dougherty, R.; Sackner, M. A. (1983a) Effect of

NO2 exposure on specific bronchial reactivity in subjects with

allergic bronchial asthma [final report]. Warren, MI: General Motors

Research Laboratories; contract report no. CR-83/07/BI.

(2) Ahmed, T.; Dougherty, R.; Sackner, M. A. (1983b) Effect of 0.1

ppm NO2 on pulmonary functions and non-specific bronchial

reactivity of normals and asthmatics [final report]. Warren, MI:

General Motors Research Laboratories; contract report no. CR-83/11/

BI.

(3) ``American Petroleum Institute v. Costle,'' 665 F. 2d 1176 (D.C.

Cir. 1981), cert. den. 102 S. Ct. 1737 (1982).

(4) Aranyi, C.; Fenters, J.; Erhlich, R.; Gardner, D. (1976)

Scanning electron microscopy of alveolar macrophages after exposure

to oxygen, nitrogen dioxide, and ozone. Environ. Health Perspect.

16: 180.

(5) Avol, E. L.; Linn, W. S.; Venet, T. G.; Hackney, J. D. (1986)

Short-term health-related effects of air pollution relatable to

power plants: a combined laboratory and field study [final report:

year 1]. Downey, CA: Rancho Los Amigos Medical Center, Environmental

Health Service; R&D series 86-RD-75.

(6) Avol, E. L.; Linn, W. S.; Peng, R. C.; Valencia, G.; Little, D.;

Hackney, J. D. (1988) Laboratory study of asthmatic volunteers

exposed to nitrogen dioxide and to ambient air pollution. Am. Ind.

Hyg. Assoc. J. 49: 143-149.

(7) Bauer, M. A.; Utell, M. J.; Morrow, P. E.; Speers, D. M.; Gibb,

F. R. (1986) Inhalation of 0.30 ppm nitrogen dioxide potentiates

exercise-induced bronchospasm in asthmatics. Am. Rev. Respir. Dis.

134: 1203-1208.

(8) Brunekreef, B.; Dockery, D. W.; Speizer, F. E.; Ware, J. H.;

Spengler, J. D.; Ferris, B. G. (1989) Home dampness and respiratory

morbidity in children. Am. Rev. Respir. Dis.140: 1,363-1,367.

(9) Bylin, G.; Lindvall, T.; Rehn, T.; Sundin, B. (1985) Effects of

short-term exposure to ambient nitrogen dioxide concentrations on

human bronchial reactivity and lung function. Eur. J. Respir. Dis.

66: 205-217.

(10) Chang, L. Y.; Graham, J. A.; Miller, F. J.; Ospital, J. J.;

Crapo, J. D. (1986) Effects of subchronic inhalation of low

concentrations of nitrogen dioxide. I. The proximal alveolar region

of juvenile and adult rats. Toxicol. Appl. Pharmacol. 83: 46-61.

(11) Coffin, D. L.; Gardner, D. E.; Sidorenko, G. I.; Pinigin, M. A.

(1977) Role of time as a factor in the toxicity of chemical

compounds in intermittent and continuous exposures. Part II. Effects

of intermittent exposure. J. Toxicol. Environ. Health 3: 821-828.

(12) D'Elia, C. F.; Sanders, J. G.; Boynton, W. R. (1986) Nutrient

enrichment studies in a coastal plain estuary: phytoplankton growth

in large-scale, continuous cultures. Can. J. Fish. Aquat. Sci. 43:

397-406.

(13) D'Elia, C. F.; Taft, J.; Smullen, J. T.; Macknis, J. (1982)

Nutrient enrichment. In: Chesapeake Bay Program technical studies: a

synthesis. Annapolis, MD: U.S. Environmental Protection Agency; pp.

36-102. Available from: NTIS, Springfield, VA; PB84-111202.

(14) De Temmerman L.; Ronse, A.; an den Cruys, K.; Meeus-Verdinne,

K.(1988) Ammonia and pine tree dieback in Belgium. In: Mathy, P.,

ed. Air pollution and ecosystems: proceedings of an international

symposium; May 1987; Grenoble, France. Boston, MA: D. Reidel

Publishing Company; pp.774-779.

(15) Dijkstra, L.; Houthuijs, D.; Brunekreef, B.; Akkerman, I.;

Boleij, J. S. M. (1990) Respiratory health effects of the indoor

environment in a population of Dutch children. Am. Rev. Respir. Dis.

142: 1172-1178.

(16) Dockery, D. W.; Spengler, J. D.; Neas, L. M.; Speizer, F. E.;

Ferris, B. G., Jr.; Ware, J. H.; Brunekreef, B. (1989a) An

epidemiologic study of respiratory health status and indicators of

indoor air pollution from combustion sources. In: Harper, J. P., ed.

Combustion processes and the quality of the indoor environment:

transactions of an international specialty conference; September

1988; Niagara Falls, NY. Pittsburgh, PA: Air & Waste Management

Association; pp. 262-271. (A&WMA transactions series:TR-15).

(17) Driscoll, C. T.; Schaefer, D. A.; Molot, L. A.; Dillon, P. J.

(1989) Summary of North American data. In: Malanchuk, J. L.;

Nilsson, J., eds. The role of nitrogen in the acidification of soils

and surface waters. Gotab, Sweden: Nordic Council of Ministers; pp.

6-1--6-45.

(18) Driscoll, C. T.; Schaefer, D. A. (1989) Background on nitrogen

processes. In: Malanchuk, J. L.; Nilsson, J., eds. The role of

nitrogen in the acidification of soils and surface waters.

Miljorapport, Sweden: Nordic Council of Ministers; pp. 4-1--4-12.

(19) Driscoll, C. T.; Van Dreason, R. (1993) Seasonal and long-term

temporal patterns in the chemistry of Adirondack lakes. Water Air

Soil Pollut. 67: 319-344.

(20) Ehrlich, R.; Henry, M. C. (1968) Chronic toxicity of nitrogen

dioxide: I. effect on resistance to bacterial pneumonia. Arch.

Environ. Health 17: 860-865.

(21) Ehrlich, R.; Findlay, J. C.; Fenters, J. D.; Gardner, D. E.

(1977) Health effects of short-term inhalation of nitrogen dioxide

and ozone mixtures. Environ. Res. 14: 223-231.

(22) Ekwo, E. E.; Weinberger, M. M.; Lachenbruch, P. A.; Huntley, W.

H. (1983) Relationship of parental smoking and gas cooking to

respiratory disease in children. Chest 84: 662-668.

(23) Ferguson, P.; Robinson, R. N.; Press, M. C.; Lee, J. A. (1984)

Element concentrations in five Sphagnum species in relation to

atmospheric pollution. J. Bryol. 13: 107-114.

(24) Fisher, T. R.; Harding, L. W., Jr.; Stanley, D. W.; Ward, L. G.

(1988a) Phytoplankton, nutrients, and turbidity in the Chesapeake,

Delaware, and Hudson estuaries. Estuarine Coastal Shelf Sci. 27: 61-

93.

(25) Folinsbee, L. J. (1992) Does nitrogen dioxide exposure increase

airways responsiveness? Toxicol. Ind. Health 8: 1-11.

(26) Friedlander, Sheldon K., Chairman, clean air Scientific

Advisory Committee (CASAC), ``Memorandum to EPA Administrator,

Subject: CASAC Review of the Air Quality Criteria Document for

Nitrogen Dioxides.'' June 19, 1981.

(27) Friedlander, Sheldon K., Chairman, Clean Air Scientific

Advisory Committee (CASAC). ``Memorandum to EPA Administrator.

Subject: CASAC Review and Closure of the OAQPS Staff Paper for

Nitrogen Oxides.'' July 6, 1982.

(28) Fujimaki, H.; Shimizu, F.; Kubota, K. (1982) Effect of subacute

exposure to NO2 on lymphocytes required for antibody responses.

Environ. Res. 29: 280-286.

(29) Gardner, D. E.; Coffin, D. L.; Pinigin, M. A.; Sidorenko, G. I.

(1977a) Role of time as a factor in the toxicity of chemical

compounds in intermittent and continuous exposures. Part I. Effects

of continuous exposure. J. Toxicol. Environ. Health 3: 811-820.

(30) Gardner, D. E.; Miller, F. J.; Blommer, E. J.; Coffin, D. L.

(1977b) Relationships between nitrogen dioxide concentration, time,

and level of effect using an animal infectivity model. In:

Dimitriades, B., ed. International conference on photochemical

oxidant pollution and its control: proceedings, v. I; September

1976; Raleigh, NC. Research Triangle Park, NC: U.S. Environmental

Protection Agency, Environmental Sciences Research Laboratory; pp.

513-525; EPA report no. EPA-600/3-77-001a. Available from: NTIS,

Springfield, VA; PB-264232. (Ecological research series).

(31) Gardner, D. E.; Miller, F. J.; Blommer, E. J.; Coffin, D. L.

(1979) Influence of exposure mode on the toxicity of NO2.

Environ. Health Perspect. 30: 23-29.

(32) Gardner, D. E.; Graham, J. A.; Illing, J. W.; Blommer, E. J.;

Miller, F. J. (1980) Impact of exposure patterns on the

toxicological response to NO2 and modifications by added

stressors. In: Proceedings of the US-USSR third joint symposium on

problems of environmental health; October 1979; Suzdal, USSR.

Research Triangle Park, NC: National Institute of Environmental

Health Sciences; pp. 17-40.

[[Page 52887]]

(33) Gardner, D. E.; Miller, F. J.; Illing, J. W.; Graham, J. A.

(1982) Non-respiratory function of the lungs: host defenses against

infection. In: Schneider, T.; Grant, L., eds. Air pollution by

nitrogen oxides: proceedings of the US-Dutch international

symposium; May; Maastricht, The Netherlands. Amsterdam, The

Netherlands: Elsevier Scientific Publishing Company; pp. 401-415.

(Studies in environmental science 21).

(34) Glezen, W. P. (1989) Antecedents of chronic and recurrent lung

disease: childhood respiratory trouble. Am. Rev. Respir. Dis. 140:

873-874.

(35) Gold, D. R.; Tager, I. B.; Weiss, S. T.; Tosteson, T. D.;

Speizer, F. E. (1989) Acute lower respiratory illness in childhood

as a predictor of lung function and chronic respiratory symptoms.

Am. Rev. Respir. Dis. 140: 877-884.

(36) Goldstein, E.; Eagle, M. C.; Hoeprich, P. D. (1973) Effect of

nitrogen dioxide on pulmonary bacterial defense mechanisms. Arch.

Environ. Health 26: 202-204.

(37) Graham, J. A.; Gardner, D. E.; Blommer, E. J.; House, D. E.;

Menache, M. G.; Miller, F. J. (1987) Influence of exposure patterns

of nitrogen dioxide and modifications by ozone on susceptibility to

bacterial infectious disease in mice. J. Toxicol. Environ. Health

21: 113-125.

(38) Hasselblad, V.; Eddy, D. M.; Kotchmar, D. J. (1992) Synthesis

of environmental evidence: nitrogen dioxide epidemiology studies. J.

Air Waste Manage. Assoc. 42: 662-671.

(39) Hazucha, M. J.; Ginsberg, J. F.; McDonnell, W. F.; Haak, E. D.,

Jr.; Pimmel, R. L.; House, D. E.; Bromberg, P. A. (1982) Changes in

bronchial reactivity of asthmatics and normals following exposures

to 0.1 ppm NO2. In: Schneider, T.; Grant, L., eds. Air

pollution by nitrogen oxides: proceedings of the US-Dutch

international symposium; May; Maastricht, The Netherlands.

Amsterdam, The Netherlands: Elsevier Scientific Publishing Company;

pp. 387-400. (Studies in environmental science 21).

(40) Hazucha, M. J.; Ginsberg, J. F.; McDonnell, W. F.; Haak, E. D.,

Jr.; Pimmel, R. L.; Salaam, S. A.; House, D. E.; Bromberg, P. A.

(1983) Effects of 0.1 ppm nitrogen dioxide on airways of normal and

asthmatic subjects. J. Appl. Physiol.: Respir. Environ. Exercise

Physiol. 54: 730-739.

(41) Howes, B. L.; Dacey, J. W. H.; Goehringer, D. D. (1986) Factors

controlling the growth form of Spartina alterniflora: feedbacks

between above-ground production, sediment oxidation, nitrogen and

salinity. J. Ecol. 74: 881-898.

(42) Husar, R. B. (1986) Emissions of sulfur dioxide and nitrogen

oxides and trends for eastern North America. In: Acid deposition:

long-term trends. Washington, DC: National Academy Press; pp. 48-92.

(43) Ito, K. (1971) [Effect of nitrogen dioxide inhalation on

influenza virus infection in mice]. Nippon Eiseigaku Zasshi 26: 304-

314.

(44) Jakab, G. J. (1987a) Modulation of pulmonary defense mechanisms

by acute exposures to nitrogen dioxide. Environ. Res. 42: 215-228.

(45) Jakab, G. J. (1987b) Modulation of pulmonary defense mechanisms

by acute exposures to nitrogen dioxide. Experientia Suppl. 51: 235-

242.

(46) Jefferies, R. L.; Perkins, N. (1977) The effects on the

vegetation of the additions of inorganic nutrients to salt marsh

soils at Stiffkey, Norfolk. J. Ecol. 65: 867-882.

(47) Johnson, D. W.; Lindberg, S. E., eds. (1992) Atmospheric

deposition and forest nutrient cycling: a synthesis of the

integrated forest study. Ecosystems. New York, NY: Springer-Verlag.

(48) Kaufmann, P. R.; Herlihy, A. T.; Mitch, M. E.; Messer, J. J.;

Overton, W. S. (1991) Stream chemistry in the eastern United States:

1. synoptic survey design, acid-base status, and regional patterns.

Water Resour. Res. 27: 611-627.

(49) Kerr, H. D.; Kulle, T. J.; McIlhany, M. L.; Swidersky, P.

(1979) Effects of nitrogen dioxide on pulmonary function in human

subjects: an environmental chamber study. Environ. Res. 19: 392-404.

(50) Klein, R. M.; Perkins, T. D. (1987) Cascades of causes and

effects of forest decline. Ambio 16: 86-93.

(51) Koenig, J. Q.; Covert, D. S.; Morgan, M. S.; Horike, M.;

Horike, N.; Marshall, S. G.; Pierson, W. E. (1985) Acute effects of

0.12 ppm ozone or 0.12 ppm nitrogen dioxide on pulmonary function in

healthy and asthmatic adolescents. Am. Rev. Respir. Dis. 132: 648-

651.

(52) Koenig, J. Q.; Pierson, W. E.; Marshall, S. G.; Covert, D. S.;

Morgan, M. S.; Van Belle, G. (1987a) The effects of ozone and

nitrogen dioxide on lung function in healthy and asthmatic

adolescents. Cambridge, MA: Health Effects Institute; research

report no. 14.

(53) Koenig, J. Q.; Covert, D. S.; Marshall, S. G.; Van Belle, G.;

Pierson, W. E. (1987b) The effects of ozone and nitrogen dioxide on

pulmonary function in healthy and in asthmatic adolescents. Am. Rev.

Respir. Dis. 136: 1152-1157.

(54) ``Lead Industries Association, Inc. v. EPA,'' 647 F. 2d 1130

(D.C. Cir. 1980), cert. den. 101 S. Ct. 621 (1980).

(55) Lee, J. A.; Press, M. C.; Woodin, S. J. (1986) Effects of

NO2 on aquatic ecosystems. In: Environment and quality of life:

study on the need for an NO2 long-term limit value for the

protection of terrestrial and aquatic ecosystems. Luxembourg:

Commission of the European Communities; pp. 99-119.

(56) Linn, W. S.; Solomon, J. C.; Trim, S. C.; Spier, C. E.; Shamoo,

D. A.; Venet, T. G.; Avol, E. L.; Hackney, J. D. (1985b) Effects of

exposure to 4 ppm nitrogen dioxide in healthy and asthmatic

volunteers. Arch. Environ. Health 40: 234-239.

(57) Linn, W. S.; Shamoo, D. A.; Avol, E. L.; Whynot, J. D.;

Anderson, K. R.; Venet, T. G.; Hackney, J. D. (1986) Dose-response

study of asthmatic volunteers exposed to nitrogen dioxide during

intermittent exercise. Arch. Environ. Health 41: 292-296.

(58) Lippmann, Morton (1984) CASAC Closure Letter to EPA

Administrator William Ruckelshaus dated October 18, 1984.

(59) Logofet, D. O.; Alexandrov, G. A. (1984) Modelling of matter

cycle in a mesotrophic bog ecosystem: II. dynamic model and

ecological succession. Ecol. Modell. 21: 259-276.

(60) Margolis, H. A.; Waring, R. H. (1986) Carbon and nitrogen

allocation patterns of Douglas-fir seedlings fertilized wih nitrogen

in autumn. II. Field performance. Can. J. For. res. 16: 903-909.

(61) McComb, A. J.; Atkins, R. P.; Birch, P. B.; Gordon, D. M.;

Lukatelich, R. J. (1981) Eutrophication in the Peel-Harvey estuarine

system, Western Australia. In: Neilson, B. J.; Cronin, L. E., eds.

Estuaries and nutrients. Clifton, NJ: Humana Press; pp. 323-342.

(62) McCurdy, T. R. (1994) Analysis of high 1 hour NO2 values

and associated annual averages using 1988-1992 data. Report of the

Office of Air Quality Planning and Standards, Durham, NC. Available

in Docket A-93-06.

(63) Melia, R. J. W.; Florey, C. du V.; Altman, D. G.; Swan, A. V.

(1977) Association between gas cooking and respiratory disease in

children. Br. Med. J. 2: 149-152.

(64) Melia, R. J. W.; Florey, C. du V.; Chinn, S. (1979) The

relation between respiratory illness in primary schoolchildren and

the use of gas for cooking: Iresults from a national survey. Int.

J. Epidemiol. 8: 333-338.

(65) Melia, J.; Florey, C.; Sittampalam, Y.; Watkins, C. (1983) The

relation between respiratory illness in infants and gas cooking in

the UK: a preliminary report. In: Air quality 6th world congress:

[proceedings of the International Union of Air Pollution Prevention

Associations]; May; Paris, France. SEPIC (APPA); pp. 263-269.

(66) Miller, F. J.; Graham, J. A.; Raub, J. A.; Illing, J. W.;

Menache, M. G.; House, D. E.; Gardner, D. E. (1987) Evaluating the

toxicity of urban patterns of oxidant gases. II. Effects in mice

from chronic exposure to nitrogen dioxide. J. Toxicol. Environ.

Health 21: 99-112.

(67) Mochitate, K.; Takahashi, Y.; Ohsumi, T.; Miura, T. (1986)

Activation and increment of alveolar macrophages induced by nitrogen

dioxide. J. Toxicol. Environ. Health 17: 229-239.

[[Page 52888]]

(68) Neas, L. M.; Ware, J. H.; Dockery, D. W.; Spengler, J. D.;

Ferris, B. G., Jr.; Speizer, F. E. (1990) The association of indoor

nitrogen dioxide levels with respiratory symptoms and pulmonary

function in children. In: Indoor air '90: proceedings of the 5th

international conference on indoor air quality and climate, volume

1, human health, comfort and performance; July-August; Toronto, ON,

Canada. Ottawa, ON, Canada: International Conference on Indoor Air

Quality and Climate, Inc.; pp. 381-386.

(69) Neas, L. M.; Dockery, D. W.; Ware, J. H.; Spengler, J. D.;

Speizer, F. E.; Ferris, B. G., Jr. (1991) Association of indoor

nitrogen dioxide with respiratory symptoms and pulmonary function in

children. Am. J. Epidemiol. 134: 204-219.

(70) Neas, L. M.; Dockery, D. W.; Spengler, J. D.; Speizer, F. E.;

Ferris, B. G., Jr. (1992) Variations in the association between

indoor nitrogen dioxide and childhood respiratory symptoms by

sampling location, season and source. Am. Rev. Respir. Dis. 145:

A93.

(71) Nixon, S. W.; Pilson, M. E. Q. (1983) Nitrogen in estuarine and

coastal marine ecosystems. In: Carpenter, E. J.; Capone, D. G., eds.

Nitrogen in the marine environment. New York, NY: Academic Press;

pp. 565-648.

(72) Ogston, S. A.; Florey, C. du V.; Walker, C. H. M. (1985) The

Tayside infant morbidity and mortality study: effect on health of

using gas for cooking. Br. Med. J. 290: 957-960.

(73) ``Oregon Natural Resource Council vs. EPA,'' No. 91-6529-HO (D.

Or.) (1993).

(74) Orehek, J.; Grimaldi, F.; Muls, E.; Durand, J. P.; Viala, A.;

Charpin, J. (1981) Response bronchique aux allergenes apres

exposition controlee au dioxyde d'azote [Bronchial response to

allergens after controlled NO2 exposure]. Bull. Eur.

Physiopathol. Respir. 17: 911-915.

(75) Parker, R. F.; Davis, J. K.; Cassell, G. H.; White, H.;

Dziedzic, D.; Blalock, D. K.; Thorp, R. B.; Simecka, J. W. (1989)

Short-term exposure to nitrogen dioxide enhances susceptibility to

murine respiratory mycoplasmosis and decreases intrapulmonary

killing of Mycoplasma pulmonis. Am. Rev. Respir. Dis. 140: 502-512.

(76) Robison, T. W.; Duncan, D. P.; Forman, H. J. (1990)

Chemoattractant and leukotriene B4 production from rat alveolar

macrophages exposed to nitrogen dioxide. Am. J. Respir. Cell Mol.

Biol. 3: 21-26.

(77) Rombout, P. J. A.; Dormans, J. A. M. A.; Marra, M.; Van Esch,

G. J. (1986) Influence of exposure regimen on nitrogen dioxide-

induced morphological changes in the rat lung. Environ. Res. 41:

466-480.

(78) Samet, J. M.; Utell, M. J. (1990) The risk of nitrogen dioxide:

what have we learned from epidemiological and clinical studies?

Toxicol. Ind. Health 6: 247-262.

(79) Samet, J. M.; Lambert, W. E.; Skipper, B. J.; Cushing, A. H.;

Hunt, W. C.; Young, S. A.; McLaren, L. C.; Schwab, M.; Spengler, J.

D. (1993) Health outcomes. In: Nitrogen dioxide and respiratory

illness in children, part I. Cambridge, MA: Health Effects

Institute; research report no. 58.

(80) Schlesinger, R. B. (1987a) Effects of intermittent inhalation

exposures to mixed atmospheres of NO2 and H2SO4 on

rabbit alveolar macrophages. J. Toxicol. Environ. Health 22: 301-

312.

(81) Schlesinger, R. B. (1987b) Intermittent inhalation of nitrogen

dioxide: effects on rabbit alveolar macrophages. J. Toxicol.

Environ. Health 21: 127-139.

(82) Silsbee, D. G.; Larson, G. L. (1982) Water quality of streams

in the Great Smoky Mountains National Park. Hydrobiologia 89: 97-

115.

(83) Simpson, J. C.; Olsen, A. R. (1990) Wet deposition temporal and

spatial patterns in North America, 1987. Research Triangle Park, NC:

U.S. Environmental Protection Agency, Atmospheric Research and

Exposure Assessment Laboratory; EPA report no. EPA-600/4-90-019.

Available from: NTIS, Springfield, VA; PB90-251836.

(84) Smith, S. V. (1984) Phosphorus versus nitrogen limitation in

the marine environment. Limnol. Oceanogr. 29: 1149-1160.

(85) Smullen, J. T.; Taft, J. L.; Macknis, J. (1982) Nutrient and

sediment loads to the tidal Chesapeake Bay system. In: Chesapeake

Bay Program technical studies: a synthesis. Annapolis, MD: U.S.

Environmental Protection Agency; pp. 150-251. Available from: NTIS,

Springfield, VA; PB84-111202.

(86) Suzuki, T.; Ikeda, S.; Kanoh, T.; Mizoguchi, I. (1986)

Decreased phagocytosis and superoxide anion production in alveolar

macrophages of rats exposed to nitrogen dioxide. Arch. Environ.

Contam. Toxicol. 15: 733-739.

(87) Tallis, J. H. (1964) Studies on southern Pennine peats: III.

the behavior of Sphagnum. J. Ecol. 52: 345-353.

(88) Tamm, C. O.; Popovic, B. (1974) Intensive fertilization with

nitrogen as a stressing factor in a spruce ecosystem. I. Soil

effects. Stockholm, Sweden: Royal College of Forestry. (Studia

forestalia suecica nr. 121).

(89) Tyler, M. (1988) Contribution of atmospheric nitrate deposition

to nitrate loading in the Chesapeake Bay. Annapolis, MD: Department

of Natural Resources, Chesapeake Bay Research & Monitoring Division;

report no. AD-88-7.

(90) U.S. Bureau of the Census. (1991) Statistical abstract of the

United States: 1991. 111th ed. Washington, DC: U.S. Bureau of the

Census; pp. 111 and 123.

(91) U.S. Department of Health and Human Services. (1990) Vital and

health statistics: current estimates from the National Health

Interview Survey, 1989. Hyattsville, MD: Public Health Service,

National Center for Health Statistics; DHHS publication no. (PHS)

90-1504. (Series 10: data from the National Health Survey no. 176).

(92) U.S. Environmental Protection Agency. (1971) Air quality

criteria for nitrogen oxides. Washington, DC: U.S. Environmental

Protection Agency, Air Pollution Control Office; EPA report no. AP-

84. Available from: NTIS, Springfield, VA; PB-197333/BE.

(93) U.S. Environmental Protection Agency. (1982) Air quality

criteria for oxides of nitrogen. Research Triangle Park, NC: Office

of Health and Environmental Assessment, Environmental Criteria and

Assessment Office; EPA report no. EPA-600/8-82-026. Available from:

NTIS, Springfield, VA; PB83-131011.

(94) U.S. Environmental Protection Agency. (1985) Ambient water

quality criteria for ammonia--1984. Washington, DC: Criteria and

Standards Division; EPA report no. EPA-440/5-85-001. Available from:

NTIS, Springfield, VA; PB85-227114.

(95) U.S. Environmental Protection Agency. (1982b) Review of the

National Ambient Air Quality Standards for Nitrogen Oxides:

Assessment of Scientific and Technical Information. OAQPS Staff

Paper. Office of Air Quality Planning and Standards; EPA report no.

EPA-450/5-82-002. Available from: NTIS, Springfield, VA.

(96) U.S. Environmental Protection Agency. (1993a) Air quality

criteria for oxides of nitrogen. Research Triangle Park, NC: Office

of Health and Environmental Assessment, Environmental Criteria and

Assessment Office; EPA report no. EPA-600/8-91/049F. Available from:

NTIS, Springfield, VA.

(97) U.S. Environmental Protection Agency. (1995) Review of the

National Ambient Air Quality Standards for Nitrogen Oxides:

Assessment of Scientific and Technical Information. OAQPS Staff

Paper. Office of Air Quality Planning and Standards; EPA report no.

EPA-452/R-95-005.

(98) U.S. Environmental Protection Agency. (1995) An SAB Report:

Review of the Acid Deposition Standard Feasibility Study Report to

Congress. Prepared by the Acid Deposition Effects Subcommittee of

the Ecological Processes and Effects Committee; EPA report no. EPA-

SAB-EPEC-95-019, September 1995.

(99) Van Breemen, N.; Van Dijk, H. F. G. (1988) Ecosystem effects of

atmospheric deposition of nitrogen in the Netherlands. In: Dempster,

J. P.; Manning, W. J.; Skeffington, R. A., eds. Excess nitrogen

deposition: [papers from the workshop]; September 1987; Leatherhead,

Surrey, United Kingdom. Environ. Pollut. 54: 249-274.

[[Page 52889]]

(100) Van Dijk, H. F. G.; De Louw, M. H. J.; Roelofs, J. G. M.;

Verburg, J. J. (1990) Impact of artificial, ammonium-enriched

rainwater on soils and young coniferous trees in a greenhouse. Part

II--effects on the trees. Environ. Pollut. 63: 41-59.

(101) Van Miegroet, H.; Cole, D. W. (1984) The impact of

nitrification on soil acidification and cation leaching in red alder

ecosystem. J. Environ. Qual. 13: 586-590.

(102) Vermeer, J. G. (1986) The effect of nutrients on shoot biomass

and species composition of wetland and hayfield communities. Acta

Oecol. Oecol. Plant. 7: 31-41.

(103) Ware, J. H.; Dockery, D. W.; Spiro, A., III; Speizer, F. E.;

Ferris, B. G., Jr. (1984) Passive smoking, gas cooking, and

respiratory health of children living in six cities. Am. Rev.

Respir. Dis. 129: 366-374.

(104) Waring, R. H. Pitman, G. B. (1985) Modifying lodgepole pine

stands to change susceptibility to mountain pine beetle attack.

Ecology 66: 889-897.

(105) White, T. C. R. (1984) The abundance of invertebrate

herbivores in relation to the availability of nitrogen in stressed

food plants. Oecologia 63:423-425.

(106) Wigington, P. J., Jr.; Davies, T. D.; Tranter, M.; Eshleman,

K. (1990) Episodic acidification of surface waters due to acidic

deposition. Washington, DC: National Acid Precipitation Assessment

Program. (Acidic deposition: state of science and technology report

12).

(107) Wolff, G. T. (1993) CASAC closure letter for the 1993 Criteria

Document for Oxides of Nitrogen addressed to U.S. EPA Administrator

Carol M. Browner dated September 30, 1993.

(108) Wolff, G. T. (1995) CASAC closure letter for the 1995 OAQPS

Staff Paper addressed to U.S. EPA Administrator Carol M. Browner

dated August 22, 1995.

(109) Yamamoto, I.; Takahashi, M. (1984) Ultrastructural

observations of rat lung exposed to nitrogen dioxide for 7 months.

Kitasato Arch. Exp. Med. 57: 57-65.

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