Ethyl Corp. v. Environmental Protection Agency

541 F.2d 1, 176 U.S. App. D.C. 373
CourtCourt of Appeals for the D.C. Circuit
DecidedMarch 19, 1976
DocketNos. 73-2205, 73-2268 to 73-2270 and 74-1021
StatusPublished
Cited by187 cases

This text of 541 F.2d 1 (Ethyl Corp. v. Environmental Protection Agency) is published on Counsel Stack Legal Research, covering Court of Appeals for the D.C. Circuit primary law. Counsel Stack provides free access to over 12 million legal documents including statutes, case law, regulations, and constitutions.

Bluebook
Ethyl Corp. v. Environmental Protection Agency, 541 F.2d 1, 176 U.S. App. D.C. 373 (D.C. Cir. 1976).

Opinions

Opinion for the court, in which Chief Judge BAZELON and Circuit Judges McGOWAN, LEVENTHAL, and SPOTTSWOOD W. ROBINSON, III, concur, filed by Circuit Judge J. SKELLY WRIGHT.

Concurring opinion, in which Circuit Judge McGOWAN joins, filed by Chief Judge BAZELON.

Concurring statement filed by Circuit Judge LEVENTHAL.

Dissenting opinion filed by Circuit Judge MacKINNON.

Dissenting opinion, in which Circuit Judges TAMM and ROBB join, filed by Circuit Judge WILKEY.

J. SKELLY WRIGHT, Circuit Judge:

Man’s ability to alter his environment has developed far more rapidly than his ability to foresee with certainty the effects of his alterations. It is only recently that we have begun to appreciate the danger posed by unregulated modification of the world around us, and have created watchdog agencies whose task it is to warn us, and protect us, when technological “advances” present dangers unappreciated — or unrevealed — by their supporters. Such agencies, unequipped with crystal balls and unable to read the future, are nonetheless charged with evaluating the effects of unprecedented environmental modifications, often made on a massive scale. Necessarily, they must deal with predictions and uncertainty, with developing evidence, with conflicting evidence, and, sometimes, with little or no evidence at all. Today we address the [379]*379scope of the power delegated one such watchdog, the Environmental Protection Agency (EPA). We must determine the certainty required by the Clean Air Act before EPA may act to protect the health of our populace from the lead particulate emissions of automobiles.

Section 211(c)(1)(A) of the Clean Air Act1 authorizes the Administrator of EPA to regulate gasoline additives whose emission products “will endanger the public health or welfare * * 42 U.S.C. § 1857f-6c(c)(l)(A). Acting pursuant to that power, the Administrator, after notice and comment, determined that the automotive emissions caused by leaded gasoline present “a significant risk of harm” to the public health. Accordingly, he promulgated regulations that reduce, in step-wise fashion, the lead content of leaded gasoline.2 We must decide whether the Administrator properly interpreted the meaning of Section 211(c)(1)(A) and the scope of his power thereunder, and, if so, whether the evidence adduced at the rule-making proceeding supports his final determination. Finding in favor of the Administrator on both grounds, and on all other grounds raised by petitioners, we affirm his determination.

I. THE FACTS, THE STATUTE, THE PROCEEDINGS, AND THE REGULATIONS

Hard on the introduction of the first gasoline-powered automobiles came the discovery that lead “antiknock” compounds, when added to gasoline, dramatically increase the fuel’s octane rating. Increased octane allows for higher compression engines, which operate with greater efficiency. Since 1928 antiknocks have been regularly added to gasoline, and a large industry has developed to supply those compounds. Today, approximately 90 percent of motor gasoline manufactured in the United States contains lead additives, even though most 1975 and 1976 model automobiles are equipped with catalytic converters, which require lead-free gasoline. From the beginning, however, scientists have questioned whether the addition of lead to gasoline, and its consequent diffusion into the atmosphere from the automobile emission, poses a danger to the public health.3 As use of [380]*380automobiles, and emission of lead particulates, has accelerated in the last quarter century, this concern has mounted. The reasons for concern are obvious (and essentially undisputed by petitioners): (1) lead in high concentrations in the body is toxic; (2) lead can be absorbed into the body from the ambient air; and (3) lead particulate emissions from gasoline engines account for approximately 90 percent of the lead in our air. Despite these apparent reasons for concern, hard proof of any danger caused by lead automotive emissions has been hard to come by. Part of the reason for this lies in the multiple sources of human exposure to lead.

Lead is an ubiquitous element. It is found in the land, in the sea, in plants, in animals, and, ultimately, in humans. Traces of lead ranging from 10 to 40 micrograms per 100 grams of blood (10-40 ug/100g)4 are found in everyone, including those living in environments with almost no atmospheric lead. National Academy of Sciences Committee on Biologic Effects of Atmospheric Pollutants, Airborne Lead in Perspective 118 (1972) (hereinafter NAS Report). Despite its universal presence, however, lead serves no known purpose in the human body, and at higher concentrations is toxic, causing anemia, severe intestinal cramps, paralysis of nerves, fatigue, and even death. Clinical symptoms of lead poisoning appear at blood lead levels of 80-100 ug or higher, and symptomatic lead poisoning may appear at levels of 50-60 ug, particularly in the presence of anemia. EPA’s Position on the Health Implications of Airborne Lead (hereinafter Third Health Document) at III — 1, Joint Appendix (hereinafter JA) 54-55.

Human body lead comes from three major sources. In most people, the largest source is the diet. EPA estimates daily dietary lead intake for adults to average 200-300 ug per day, with a range of 100-500 ug a day. Third Health Document at V-2, JA 82. Absorption of dietary lead into the bloodstream is estimated at about 10 percent, although in children absorption may be as high as 50 percent. Thus the average adult adds 20-30 ug of lead to his bloodstream daily from his diet alone. This daily intake, which may be highly variable depending on individual diets, NAS Report at 50, is generally regarded as, for all practical purposes, uncontrollable.5

A second major source of the body’s lead burden, at least among urban children, is regarded as controllable, although effective control may be both difficult and expensive to achieve. Ingestion of lead paint by children with pica (the abnormal ingestion of non-food substances, a relatively common trait in pre-school children, particular ages 1-3) is generally regarded as “the principal environmental source in cases of severe acute lead poisoning in young children.” NAS Report at 140. Lead-based paint was widely used in pre-1940 housing, for both interiors and exteriors, so children living in older housing, particularly in urban ghettos where such paint is both present and peeling, are most susceptible to this form of lead poisoning. Limited control has been achieved in that lead paints are now rarely [381]*381used, and are frequently banned by statute, for interior surfaces. But while some local laws require removal of existing peeling lead paints, and there is federal legislation to aid states and municipalities in such efforts, Lead-Based Paint Poisoning Prevention Act, 42 U.S.C. §§ 4801 et seq. (1970), there is no concentrated national effort at removal, and the danger to children living in dilapidated housing will remain for some time.6

The last remaining major source of lead exposure for humans is the ambient air.

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Bluebook (online)
541 F.2d 1, 176 U.S. App. D.C. 373, Counsel Stack Legal Research, https://law.counselstack.com/opinion/ethyl-corp-v-environmental-protection-agency-cadc-1976.