[Federal Register Volume 60, Number 196 (Wednesday, October 11, 1995)]
[Proposed Rules]
[Pages 52874-52889]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 95-25179]



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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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