Lead Industries Association, Inc. v. Environmental Protection Agency, Bunker Hill Company, Intervenor. St. Joe Minerals Corporation v. Environmental Protection Agency, Bunker Hill Company, Intervenor

This is the third occasion on which this court has been asked to review Environmental Protection Agency (EPA or Agency) regulations promulgated under authority of the Clean Air Act, as amended, 42 U.S.C. § 7401 et seq. (Supp. I 1977) (the Act), and specifically designed to deal with the health problems associated with lead in the ambient air. In Amoco Oil Co. v. EPA, 501 F.2d 722 (D.C.Cir.1974), we upheld regulations prohibiting the sale of leaded gasoline for use in automobiles equipped with "catalytic converter" devices for controlling exhaust emissions and requiring widespread retail marketing of at least one grade of unleaded gasoline. And in Ethyl Corp. v. EPA, 541 F.2d 1 (D.C.Cir.) (en banc ), cert. denied, 426 U.S. 941, 96 S.Ct. 2663, 49 L.Ed.2d 394 (1976), we affirmed an EPA order requiring annual reductions in the lead content of leaded gasoline. In the present consolidated cases we are asked to review EPA regulations establishing national ambient air quality standards for lead. These air quality standards prescribe the maximum concentrations of lead that will be permitted in the air of our country. We must decide whether EPA's Administrator acted within the scope of his statutory authority in promulgating these regulations and, if so, whether the evidence adduced at the rulemaking proceeding supports his final determinations. In addition, we must examine the petitioners' claims that infirmities in the procedures employed by EPA in this rulemaking warrant remand of the regulations to the Agency. Petitioners are the Lead Industry Association, Inc. (LIA), a nonprofit trade association whose 78 members include most of the country's producers and commercial consumers of lead (No. 78-2201), and St. Joe Minerals Corporation (St. Joe) (No. 78-2220).1

Man's ability to alter his environment to achieve perceived goals has undoubtedly made an enormous contribution to his economic and social well-being. This undertaking is not, however, without attendant costs. One of these costs is the toll that these alterations may exact on the environment itself and, in turn, the dangers that this may pose for the public health and welfare. Unfortunately, man's ability to alter the environment often far outstrips his ability to foresee with any degree of certainty what untoward effects these changes may bring. The issues presented by these cases illustrate this sad fact.

Lead's environmental significance is a consequence of both its abundance and its utility. The relative abundance of lead in the earth's crust makes it unique among the toxic heavy metals. EPA's "Air Quality Criteria For Lead" (hereinafter cited as CD) 1-1, Joint Appendix (JA) 1105. And centuries of mining and smelting, and the use of lead in a variety of human activities, have increased the natural background concentration of lead in the environment. Id. But it is only since the industrial age and the use of lead as a gasoline additive that lead has become pervasive. Id. at 1-2 1-3, JA 1106-1107. Today lead is ubiquitous. It is found in almost every medium with which we come into contact food, water, air, soil, dust, and paint, id. 1-1, JA 1105, each of which represents a potential pathway for human lead exposure through ingestion or inhalation. The widespread presence of this toxic metal in the environment poses a significant health risk. Lead is a poison which has no known beneficial function in the body, id. 1-12, JA 1116, but when present in the body in sufficient concentrations lead attacks the blood, kidneys, and central nervous and other systems and can cause anemia, kidney damage, severe brain damage, and death. Id. 1-6 1-9, JA 1110-1113.2

There are three major sources of the body's lead burden. In most people the largest source is diet. CD 7-9, JA 1179.3 Another source, particularly in children, is the habit of placing hands, objects, and materials in the mouth.4 The third major source is the ambient air; airborne lead is deposited in the respiratory tract as a person breathes lead-contaminated air and is subsequently absorbed into the bloodstream. CD 1-5, JA 1108. Once the lead is in the bloodstream its source is immaterial; total lead intake is the sum of the intake from all these sources. The multiplicity of sources of lead intake increases the difficulty of controlling human lead exposure. Much of the protective activity in this area has focused on limiting the amount of lead in the ambient air, the most controllable source of lead exposure. In this country, by far the largest source of lead emissions accounting for 88 percent of total lead emissions according to EPA estimates is the exhaust of motor vehicles powered by gasoline containing lead additives. CD 5-3, JA 1140. Another eight percent of lead emissions is the result of solid waste incineration and combustion of waste oil. Id. Industrial facilities account for the remaining four percent of total lead emissions. Id.

Acting pursuant to authority conferred on it by Congress in the Clean Air Act, as amended, 42 U.S.C. § 7401 et seq., EPA has been involved in regulation of lead emissions almost since the Agency's inception.5 Its initial approach to controlling the amount of lead in the ambient air was to limit lead emissions from automobiles by restricting the amount of lead in gasoline. To this end it promulgated the regulations which we upheld in Amoco Oil Corp. v. EPA, supra, and Ethyl Corp. v. EPA, supra. However, in 1975 the Natural Resources Defense Council, Inc. (NRDC), and others brought suit against EPA claiming that the Agency was required by Section 108 of the Clean Air Act, 42 U.S.C. § 7408, to list lead as a pollutant for which an air quality criteria document would be prepared, and for which national ambient air quality standards should be promulgated under Section 109 of the Act, 42 U.S.C. § 7409. The District Court agreed with NRDC and directed the Administrator to list lead as a pollutant under Section 108 of the Act, by March 31, 1976. Natural Resources Defense Council, Inc. v. Train, 411 F.Supp. 864 (S.D.N.Y.1976). The Second Circuit affirmed, 545 F.2d 320 (2d Cir. 1976), and EPA initiated the proceedings outlined in the statute which are under review here.

The first step toward establishing national ambient air quality standards for a particular pollutant is its addition to a list, compiled by EPA's Administrator, of pollutants that cause or contribute to air pollution "which may reasonably be anticipated to endanger public health or welfare(.)" Section 108(a)(1), 42 U.S.C. § 7408(a)(1). Within twelve months of the listing of a pollutant under Section 108(a) the Administrator must issue "air quality criteria" for the pollutant. Section 108 makes it clear that the term "air quality criteria" means something different from the conventional meaning of "criterion"; such "criteria" do not constitute "standards" or "guidelines," but rather refer to a document to be prepared by EPA which is to provide the scientific basis for promulgation of air quality standards for the pollutant. This criteria document must "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 such pollutant in the ambient air, in varying quantities." Section 108(a)(2), 42 U.S.C. § 7408(a)(2).

At the same time as he issues air quality criteria for a pollutant, the Administrator must also publish proposed national primary and secondary air quality standards for the pollutant. Section 109(a)(2), 42 U.S.C. § 7409(a) (2). National primary ambient air quality standards are standards "the attainment and maintenance of which in the judgment of the Administrator, based on such criteria and allowing an adequate margin of safety, are requisite to protect the public health." Section 109(b)(1), 42 U.S.C. § 7409(b)(1). Secondary air quality standards "specify a level of air quality the attainment and maintenance of which in the judgment of the Administrator, based on such criteria, is requisite to protect the public welfare from any known or anticipated adverse effects associated with the presence of such air pollutant in the ambient air." Section 109(b)(2), 42 U.S.C. § 7409(b)(2). Effects on "the public welfare" include "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." Section 302(h), 42 U.S.C. § 7602(h). The Administrator is required to submit the proposed air quality standards for public comment in a rulemaking proceeding, the procedure for which is prescribed by Section 307(d) of the Act, 42 U.S.C. § 7607(d).

Within six months of publication of the proposed standards the Administrator must promulgate final primary and secondary ambient air quality standards for the pollutant. Section 307(d)(10), 42 U.S.C. § 7607(d)(10). Once EPA has promulgated national ambient air quality standards, responsibility under the Act shifts from the federal government to the states. Within nine months of promulgation of the standards each state must prepare and submit to EPA for approval a state implementation plan. Section 110(a)(1), 42 U.S.C. § 7410(a) (1). These state implementation plans must contain emission limitations and all other measures necessary to attain the primary standards "as expeditiously as practicable," but no later than three years after EPA approval of the plan, and to attain the secondary standards within a reasonable period of time. Section 110(a)(2)(A) & (B), 42 U.S.C. § 7410(a)(2)(A) & (B). The Administrator is authorized to extend the deadline for attainment of the primary air quality standards by two years, but thereafter it must be met. Section 110(e), 42 U.S.C. § 7410(e).

III. THE LEAD STANDARDS RULEMAKING PROCEEDINGS

As required by statute, EPA's first step toward promulgating air quality standards for lead was to prepare a criteria document. The Lead Criteria Document was the culmination of a process of rigorous scientific and public review, and thus is a comprehensive and thoughtful analysis of the most current scientific information on the subject. The Lead Criteria Document went through three major drafts, and three separate reviews, including public meetings by the Subcommittee on Scientific Criteria for Environmental Lead of EPA's Science Advisory Board (SAB Lead Subcommittee).6 The Agency reviewed over 280 public comments, most of a sophisticated scientific nature, before it issued the final Criteria Document. Members of the public, industry (including the petitioners in these cases), environmental groups, the scientific community, and state and federal government agencies actively participated in the review of the drafts. Notice of the meetings of the SAB Lead Subcommittee was published in the Federal Register, and the drafts of the Criteria Document which were to be reviewed were available before the meetings. A formal record and a transcript of the proceedings were kept, and a review of the transcript shows that scientists with differing views could and did exchange ideas with each other as well as agency staff, and that all were questioned by the members of the Subcommittee.

EPA released its "Air Quality Criteria For Lead" on December 14, 1977. 42 Fed.Reg. 63076, JA 1480. The document was "prepared to reflect the current state of knowledge about lead specifically, those issues that are most relevant to establishing the objective scientific data base that will be used to recommend an air quality standard for lead that will adequately safeguard the public health." CD 1-1, JA 1105. Accordingly, the Criteria Document examined a large number of issues raised by the problem of lead in the environment. One of these was the effects of lead exposure on human health. The Criteria Document concluded that, among the major organ systems, the hematopoietic (blood-forming) and neurological systems are the areas of prime concern. CD 1-12, JA 1116. Its discussion of the effects of lead on these two organ systems is central to our review of the lead standards.8

The Criteria Document identified a variety of effects of lead exposure on the blood-forming system. We will discuss only the effects that played an important role in the Administrator's analysis. Anemia, which can be caused by lead-induced deformation and destruction of erythrocytes (red blood cells) and decreased hemoglobin synthesis,9 is often the earliest clinical manifestation of lead intoxication. CD 11-7, 11-8, 11-13, JA 1229-1230, 1235. Symptoms of anemia include pallor of the skin, shortness of breath, palpitations of the heart, and fatigability.10 The Criteria Document concluded, after a review of various studies, that in "children, a threshold level for anemia is about 40 u(g) Pb/dl, whereas the corresponding value for adults is about 50 ug Pb/dl." CD 11-13, JA 1235. (The concentration of lead in the blood is measured in micrograms of lead per deciliter of blood ug Pb/dl.)

The Criteria Document also examined other more subtle effects on the blood-forming system, associated with lower levels of lead exposure. The most pertinent of these "subclinical"11 effects for purposes of these cases is lead-related elevation of erythrocyte protoporphyrin (EP elevation).12 According to the Criteria Document, this phenomenon must, for a number of reasons, be regarded as an indication of an impairment of human health. CD 11-11, JA 1233. First, EP elevation indicates an impairment in the functioning of the mitochondria, the subcellular units which play a crucial role in the production of energy in the body, and in cellular respiration. CD 1-6, 11-11, 11-14, 13-5, JA 1110, 1233, 1236, 1335. Second, it indicates that lead exposure has begun to affect one of the basic biological functions of the body production of heme within the red blood cells.13 Heme is critical to transporting oxygen to every cell in the body. Third, EP elevation may indicate that any reserve capacity there may be in the heme synthesis system has been reduced. CD 11-11, JA 1233. Finally, the Criteria Document noted that lead's interference with the process of heme synthesis in the blood may suggest that lead interferes with production of heme proteins in other organ systems, particularly the renal and neurological systems. CD 11-11, JA 1233. The Criteria Document reported that the threshold for EP elevation in children and women is at blood lead levels of 15-20 ug Pb/dl, and 25-30 ug Pb/dl in adult males. CD 13-8 (Table 13-2), JA 1338 (Table 13-2). While suggesting that some of the initial hematological effects of lead exposure may constitute relatively mild effects at low blood lead levels, the Criteria Document concluded that "they nevertheless signal the onset of steadily intensifying adverse effects as blood lead elevations increase. Eventually, (these) * * * effects reach such magnitude that they are of clearcut medical significance as indicators of undue lead exposure." CD 1-13, JA 1117. The Criteria Document did not identify a particular blood lead level at which regulatory response was appropriate, but it did note with approval the 1975 guidelines issued by the Center For Disease Control, which use elevated EP at blood lead levels of 30 ug Pb/dl as the cut-off point in screening children for lead poisoning. CD 13-5, JA 1335.

The Criteria Document also examined the effects of lead exposure on the central nervous system. Among the most deleterious effects of lead poisoning are those associated with severe central nervous system damage at high exposure levels. The Criteria Document noted that neurological and behavioral deficits have long been known to be among the more serious effects of lead exposure, but it pointed out that there is disagreement about whether these effects are reversible, and about what exposure levels are necessary to produce specific deleterious effects. CD 11-14, JA 1236. Much of the impetus for the debate on these questions has been provided by the continual emergence of new information suggesting that lead exposure levels previously thought to be harmless actually cause significant neurological damage. Id. The more severe neurological effects of high level lead exposure are the clinical syndrome of lead encephalopathy. Early symptoms include dullness, restlessness, irritability, headaches, muscular tremor, hallucinations, and loss of memory. These symptoms rapidly progress (sometimes within 48 hours) to delirium, mania, convulsions, paralysis, coma, and death. Id. at 11-15, JA 1237. The Criteria Document expressed particular concern that the onset of these serious symptoms can be quite abrupt, even in the absence of prior overt or clinical symptoms of disease. Id. at 13-6, JA 1336. After a review of various studies, the Criteria Document concluded that the blood lead threshold for these neurological effects of high level exposure is 80-100 ug Pg/dl in children, and 100-200 ug Pb/dl in adults. Id. at 1-13, 11-18, 11-25, 13-6, JA 1117, 1240, 1247, 1336.

The Criteria Document also went on to consider the evidence on whether lower level lead exposures can affect the central nervous system, particularly in children. It acknowledged that the issue is unsettled and somewhat controversial, but it was able to conclude, after a careful review of various studies on the subject,14 that "a rather consistent pattern of impaired neural and cognitive functions appears to be associated with blood lead levels below those producing the overt symptomatology of lead encephalopathy." CD 1-7, JA 1111. The Criteria Document reported that "(t)he blood lead levels at which neurobehavioral deficits occur in otherwise asymptomatic children appear to start at a range of 50 to 60 ug/dl, although some evidence tentatively suggests that such effects may occur at slightly lower levels for some children." Id.15

In addition to examining the health effects of lead exposure, the Criteria Document also discussed other issues critical to the task of setting air quality standards for lead. One of these issues is the relationship between air lead exposure and blood lead levels a relationship commonly referred to as the air lead/blood lead ratio. The Criteria Document acknowledged that derivation of a functional relationship between air lead exposure and blood lead levels is made difficult by the fact that the relationship is not a linear one; rather, the ratio tends to increase as air lead levels are reduced, CD 12-24, JA 1311. The Document was nevertheless able to conclude, after a detailed examination of the relevant studies, CD 12-22 12-29, JA 1309-1316, that air lead/blood lead ratios fall within a range of 1:1 to 1:2 (ug Pb/m 3 air):(ug Pb/dl blood) at the levels of lead exposure generally encountered by the population, i.e., blood lead levels increase by between 1 and 2 ug Pb/dl of blood for every 1 ug Pb/m 3 of air. (Air lead content is measured in micrograms of lead per cubic meter of air ug Pb/m 3.) CD 12-38, JA 1325. The Criteria Document reported that the studies indicate that the ratio for children is at the upper end of this range or even slightly above it. Id.

Finally, the Criteria Document also examined the distribution of blood lead levels throughout the population, concluding that there is a significant variability in individual blood lead responses to any particular level of air lead exposure. It further found that this variability is consistent and predictable, and that the application of established statistical techniques to the distribution of individual blood lead levels would make it possible to predict what proportion of the population would be above or below any particular blood lead level at a given level of air lead exposure.16 The Criteria Document looked into the question whether any sub-groups within the population are particularly vulnerable to the effects of lead exposure. It concluded that preschool-age children and pregnant women are particularly sensitive to lead exposure, the latter mainly because of the risk to the unborn child. CD 13-11 13-14, JA 1341-1344.

Simultaneously with the publication of the Lead Criteria Document on December 14, 1977, the Administrator proposed a national primary ambient air quality standard for lead of 1.5 ug Pb/m 3 monthly average. 42 Fed.Reg. 63076, JA 1480. He also proposed that the secondary air quality standard be set at the same level as the primary standard because the welfare effects associated with lead exposure did not warrant imposition of a stricter standard. 42 Fed.Reg. 63081-63082, JA 1485-1486. In the preamble to the proposed standards the Administrator explained the analysis EPA had employed in setting the standards.

The Administrator first pointed out that a number of factors complicate the task of setting air quality standards which will protect the population from the adverse health effects of lead exposure. First, some sub-groups within the population have a greater potential for, or are more susceptible to the effects of, lead exposure. Id. at 63077, JA 1481. Second, there are a variety of adverse health effects associated with various levels of lead exposure. Id. Third, the variability of individual responses to lead exposure, even within particular sub-groups of the population, would produce a range of blood lead levels at any given air lead level. Id. at 63079, JA 1483. Fourth, airborne lead is only one of a number of sources of lead exposure and the relative contribution from each source is difficult to quantify. Id. at 63080, JA 1484. Finally, the relationship between air lead exposure and blood lead levels is a complex one. Id. at 63079, JA 1483.

In response to the first problem the Administrator began by noting that protection of the most sensitive groups within the population had to be a major consideration in determining the level at which the air quality standards should be set. And he determined that children between the ages of 1 and 5 years are most sensitive to the effects of lead exposure both because the hematologic and neurologic effects associated with lead exposure occur in children at lower threshold levels than in adults, and because the habit of placing hands and other objects in the mouth subjects them to a greater risk of exposure. Id. at 63077-63078, JA 1481-1482. Next, the Administrator examined the various health effects of lead exposure and proposed that EP elevation should be considered the first adverse health effect of lead exposure because it indicates an impairment of cellular functions, and should be the pivotal health effect on which the lead standards are based. Id. at 63078, JA 1482. Accordingly, he proposed that the air lead standards be designed to prevent the occurrence of EP elevation in children. In order to accomplish this, and to address the problem of variable responses to lead exposure, the Administrator selected 15 ug Pb/dl, the lowest reported threshold blood lead level for EP elevation in children, as the target mean population blood lead level.17 He reasoned that setting the target mean population blood lead level at the lowest reported threshold blood lead level for EP elevation would ensure that most of the target population would be kept below blood lead levels at which adverse health effects occur. Id. at 63078, JA 1483. The Administrator also discussed the alternative approaches of basing the standard on more severe effects such as anemia, or attempting to decide the actual level of EP elevation which represents an adverse effect on health, and then making an adjustment to allow a margin of safety. Id. He specifically invited comments on these alternative approaches. Id. Finally, the Administrator outlined another approach to calculating the target mean population blood lead level involving the use of statistical techniques discussed in the Criteria Document. Id.18

Having selected a target mean population blood lead level, the Administrator's next step was to allow for the multiplicity of sources of lead exposure. He thus had to estimate the amount of blood lead that should be attributed to non-air sources. The Administrator admitted that any amount he selected could be no more than a theoretical national average, and on the basis of the evidence available he proposed that the lead standards should be based on the general assumption that 12 ug Pb/dl of blood lead should be attributed to non-air sources. Id. at 63080-63081, JA 1484-1485. Given the target mean population blood lead level of 15 ug Pb/dl and the assumed contribution from non-air sources of 12 ug Pb/dl, the maximum allowable contribution from ambient air is 3 ug Pb/dl. The final step in his analysis was to determine what air lead level would prevent the ambient air contribution to blood lead levels from exceeding 3 ug Pb/dl. This step required determining the relationship between air lead exposure and blood lead levels, i.e., the air lead/blood lead ratio. On the basis of the information in the Criteria Document, the Administrator selected a ratio of 1:2 as appropriate for calculating the effect of air lead exposure on blood lead levels in children. Id. at 63079, JA 1483.

Thereafter, calculation of the air quality standard was a mathematical exercise as shown in the following table.

1.                            Target mean blood lead level         15 ug Pb/dl
2.                            Assumed non-air contribution        -12 ug Pb/dl
                                                                  -------------
3.                            Allowable air contribution          =3 ug Pb/dl
4.                            Permissible air lead concentration
                              given assumed air lead/blood lead
                              ratio
                              3 ug Pb/dl X 1 ug Pbm 3 air         =1.5 ug Pb/m
                                                                    3
            ----------------  2 ug Pb/dl blood

The Administrator concluded, on the basis of available information, that the averaging period for the lead standard should be a calendar month. Id. at 63081, JA 1485.

The public comment period ran from December 14, 1977 to March 17, 1978, and public hearings on the proposed standards were held on February 15 and 16, 1978. 43 Fed.Reg. 46246, JA 2948. The comments on the proposed standards were sharply divided. The comments submitted by the lead industry and its experts uniformly opposed the proposed standards, and many endorsed a standard of 5 ug Pb/m 3, the standard proposed in the discredited first draft of the Criteria Document, see note 7 supra, as adequate to protect the public health. 43 Fed.Reg. 46248, JA 2950. On the other hand, environmental groups, medical experts, and state, local, and federal agencies either endorsed the proposed standards or called for even stricter standards. Id. None of the comments seriously questioned the selection of children between the ages of 1 and 5 years as the target population group, or the estimate of a contribution from non-air sources of 12 ug Pb/dl. The major areas of controversy were the Administrator's choice of EP elevation as the pivotal adverse health effect and his conclusion that the threshold blood lead level for EP elevation in children is 15 ug Pb/dl, the selection of an appropriate air lead/blood lead ratio, the appropriate allowance for an adequate margin of safety, and the averaging time period for the standards. Id.19

A number of comments challenged the selection of EP elevation as the pivotal adverse health effect, insisting that EP elevation merely indicates a biological change or response which is in no way harmful to health,20 and in addition they criticized the Administrator's determination that the blood lead threshold for EP elevation in children is 15 ug Pb/dl.21 These comments suggested that a decrease in hemoglobin levels, which begins at blood lead levels no lower than 40 ug Pb/dl, should be the pivotal adverse health effect on which the standards are based.22 Other experts, however, agreed with the Administrator's conclusion that EP elevation must be considered an adverse health effect of lead exposure, and argued that using EP elevation as the pivotal adverse health effect would, in addition, allow an adequate margin of safety in protecting against the more serious health effects associated with higher levels of lead exposure.23 Finally, several industry experts appeared to indicate a preference for the lognormal statistical procedures that the Administrator had, in the proposed standards, suggested as an alternative method for determining the target mean population blood lead level.24

The Administrator promulgated the final air quality standards on October 5, 1978, prescribing national primary and secondary ambient air quality standards for lead of 1.5 ug Pb/m 3, averaged over a calendar quarter. 43 Fed.Reg. 46246, JA 2948. Although the final standards were the same as the proposed standards (with the exception of the change in the averaging period from 30 to 90 days), the Administrator arrived at the final standards through somewhat different analysis. The preamble to the final standards reveals that the comments on the proposed standards had led the Administrator to reconsider his analysis. In particular, he seemed to feel that legitimate questions had been raised concerning the health significance of the early stages of EP elevation and about the threshold blood lead level for this condition. 43 Fed.Reg. 46248, 46253, JA 2950, 2955. The Administrator's reexamination focused on two key questions: (1) What is the maximum safe individual blood lead level for children? and (2) what proportion of the target population should be kept below this blood lead level? Id. at 46249, 46252-46253, JA 2951, 2954-2955. Addressing the first issue required a review of the health effects of lead exposure discussed in the Criteria Document. The Administrator concluded that, although EP elevation beginning at blood lead levels of 15-20 ug Pb/dl is potentially adverse to the health of children, only when blood lead concentration reaches a level of 30 ug Pb/dl is this effect significant enough to be considered adverse to health. Id. at 46253, JA 2955. Accordingly, he selected 30 ug Pb/dl as the maximum safe individual blood lead level for children. Id. The Administrator based this choice on three mutually supporting grounds. First, it is at this blood lead level that the first adverse health effect of lead exposure impairment of heme synthesis begins to occur in children. Second, a maximum safe individual blood lead level of 30 ug Pb/dl would allow an adequate margin of safety in protecting children against more serious effects of lead exposure anemia, symptoms of which begin to appear in children at blood lead levels of 40 ug Pb/dl, and central nervous system deficits which start to occur in children at blood lead levels of 50 ug Pb/dl. Third, the Administrator reasoned that the maximum safe individual blood lead level should be no higher than the blood lead level used by the Center for Disease Control in screening children for lead poisoning 30 ug Pb/dl. Id.

Having determined the maximum safe individual blood lead level for the target population, the Administrator next focused on the question of what percentage of children between the ages of 1 and 5 years the standard should attempt to keep below this blood lead level. According to the 1970 census, there are approximately 20 million children under the age of 5 years in the United States, 12 million of them in urban areas and 5 million in inner cities where lead exposure may be especially high. The Administrator concluded that in order to provide an adequate margin of safety, and to protect special high risk sub-groups, the standards should aim at keeping 99.5% of the target population below the maximum safe individual blood lead level of 30 ug Pb/dl.25 Id. at 46253, 46255, JA 2955, 2957. The next step in the analysis was to determine what target mean population blood lead level would ensure that 99.5% of the children below the age of 5 years would be kept below the maximum safe individual blood lead level of 30 ug Pb/dl. Using the lognormal statistical technique he had alluded to in the proposed standards,26 he calculated that a target mean population blood lead level of 15 ug Pb/dl (the same number as in the proposed standards, but arrived at through different analysis), would accomplish this task.27 Id. at 46253, 46254, JA 2955, 2956. Thereafter, the Administrator used the same estimate of the contribution from non-air sources, 12 ug Pb/dl, and the same air lead/blood lead ratio, 1:2, that he had used in calculating the proposed standards,28 to compute the final ambient air quality standards for lead. The result was an ambient air quality standard of 1.5 ug Pb/m 3, the same as the proposed standard. Id. at 46254, JA 2956. The Administrator did, however, change the averaging period for the standards from one calendar month to one calendar quarter, id. at 46255, JA 2957, because he felt that this change would significantly improve the validity of the data to be used in monitoring the progress toward attainment of the standards without rendering the standards less protective. Id.

On December 8, 1978 LIA petitioned EPA for reconsideration and a stay of the lead standards. JA 2980-3000. The Administrator denied the petition on February 2, 1979. JA 3001-3007. These petitions for review of the lead standards regulations followed. Before examining the petitioners' challenges to the regulations, we consider the limits of our reviewing function.

The scope of judicial review of the Administrator's decisions and actions is delineated by Section 307(d) of the Act, 42 U.S.C. § 7607(d). We must uphold the Administrator's actions unless we find that they were: (1) "arbitrary, capricious, an abuse of discretion, or otherwise not in accordance with law"; (2) "contrary to constitutional right, power, privilege, or immunity"; (3) "in excess of statutory jurisdiction, authority, or limitations, or short of statutory right(.)" Section 307(d)(9), 42 U.S.C. § 7607(d)(9). In addition, we may set aside any action found to be "without observance of procedure required by law," if (i) the failure to follow the prescribed procedure was arbitrary or capricious, (ii) the procedural objection was raised during the public comment period, or there were good reasons why it was not, and (iii) the procedural errors "were so serious and related to matters of such central relevance to the rule that there is a substantial likelihood that the rule would have been significantly changed if such errors had not been made." Id. Section 307(d)(8), 42 U.S.C. § 7607(d)(8).

These statutory provisions and a considerable body of case law demonstrate that our role as a reviewing court is limited. The "arbitrary and capricious" standard of review is highly deferential, and presumes agency action to be valid. Citizens to Preserve Overton Park, Inc. v. Volpe, 401 U.S. 402, 415, 91 S.Ct. 814, 823, 28 L.Ed.2d 136 (1971); Ethyl Corp. v. EPA, supra, 541 F.2d at 34. Moreover, the reviewing court may not substitute its judgment for the agency's, Citizens to Preserve Overton Park, Inc. v. Volpe, supra, 401 U.S. at 416, 91 S.Ct. at 823, and must affirm the agency's decision if a rational basis for it is presented. Bowman Transportation, Inc. v. Arkansas-Best Freight Systems, Inc., 419 U.S. 281, 290, 95 S.Ct. 438, 444, 42 L.Ed.2d 447 (1974); United States v. Allegheny-Ludlum Steel Corp., 406 U.S. 742, 749, 92 S.Ct. 1941, 1946, 32 L.Ed.2d 453 (1972). Of course a reviewing court does not serve as a mere rubber stamp for agency decisions. Rather, the function of judicial review is to ensure that agency decisions are "based on a consideration of the relevant factors." Citizens to Preserve Overton Park, Inc. v. Volpe, supra, 401 U.S. at 416, 91 S.Ct. at 824.

In addition, the court must undertake a "substantial inquiry" into the facts, one that is "searching and careful."