Daily Rules, Proposed Rules, and Notices of the Federal Government
This action also presents our decision regarding the February 28, 2002 petition for rulemaking submitted by the Cement Kiln Recycling Coalition, relating to EPA's implementation of the so-called omnibus permitting authority under section 3005(c) of the Resource Conservation and Recovery Act (RCRA). That section requires that each permit issued under RCRA contain such terms and conditions as permit writers determine to be necessary to protect human health and the environment. In that petition, the Cement Kiln Recycling Coalition requested that we repeal the existing site-specific risk assessment policy and technical guidance for hazardous waste combustors and that we promulgate the policy and guidance as rules in accordance with the Administrative Procedure Act if we continue to believe that site-specific risk assessments may be necessary.
The promulgation of the final rule would affect the following North American Industrial Classification System (NAICS) and Standard Industrial Classification (SIC) codes:
This table is not intended to be exhaustive, but rather provides a guide for readers regarding entities likely to be regulated by this action. This table lists examples of the types of entities EPA is now aware could potentially be regulated by this action. Other types of entities not listed could also be affected. To determine whether your facility, company, business, organization, etc., is regulated by this action, you should examine the applicability criteria in Part II of this preamble. If you have any questions regarding the applicability of this action to a particular entity, consult the person listed in the preceding
Section 112 of the Clean Air Act requires that the EPA promulgate regulations requiring the control of HAP emissions from major and certain area sources. The control of HAP is achieved through promulgation of emission standards under sections 112(d) and (in a second round of standard setting) (f).
EPA's initial list of categories of major and area sources of HAP selected for regulation in accordance with section 112(c) of the Act was published in the
Today's notice finalizes standards for controlling emissions of HAP from hazardous waste combustors: incinerators, cement kilns, lightweight aggregate kilns, boilers, process heaters
Phase I combustor sources are regulated under the Resource Conservation and Recovery Act (RCRA), which establishes a “cradle-to-grave” regulatory structure overseeing the safe treatment, storage, and disposal of hazardous waste. We issued RCRA rules to control air emissions from hazardous waste burning incinerators in 1981, 40 CFR Parts 264 and 265, Subpart O, and from cement kilns and lightweight aggregate kilns that burn hazardous waste in 1991, 40 CFR Part 266, Subpart H. These rules rely generally on risk-based standards to assure control necessary to protect human health and the environment, the applicable RCRA standard. See RCRA section 3004 (a) and (q).
The Phase I source categories also are subject to standards under the Clean Air Act. We promulgated standards for Phase I sources on September 30, 1999 (64 FR 52828). This final rule is referred to in this preamble as the Phase I rule or 1999 final rule. These emission standards created a technology-based national cap for hazardous air pollutant emissions from the combustion of hazardous waste in these devices. The rule regulates emissions of numerous hazardous air pollutants: dioxin/furans, other toxic organics (through surrogates), mercury, other toxic metals (both directly and through a surrogate), and hydrogen chloride and chlorine gas. Where necessary, Section 3005(c)(3) of RCRA provides the authority to impose additional conditions on a source-by-source basis in a RCRA permit if necessary to protect human health and the environment.
A number of parties, representing interests of both industrial sources and of the environmental community, sought judicial review of the Phase I rule. On July 24, 2001, the United States Court of Appeals for the District of Columbia Circuit granted portions of the Sierra Club's petition for review and vacated the challenged portions of the standards.
Acting on this invitation, all parties moved the Court jointly to stay the issuance of its mandate for four months to allow EPA time to develop interim standards, which would replace the vacated standards temporarily, until final standards consistent with the Court's mandate are promulgated. The interim standards were published on February 13, 2002 (67 FR 6792). EPA did not justify or characterize these standards as conforming to MACT, but rather as an interim measure to prevent adverse consequences that would result from the regulatory gap resulting from no standards being in place. Id. at 6793, 6795-96; see also 69 FR at 21217 (April 20, 2004). EPA also entered into a settlement agreement, enforceable by the Court of Appeals, to issue final standard conforming to the Court's mandate by June 14, 2005. That date has since been extended to September 14, 2005.
Phase II combustors—boilers and hydrochloric acid production furnaces—are also regulated under the Resource Conservation and Recovery Act (RCRA) pursuant to 40 CFR Part 266, Subpart H, and (for reasons discussed below) are also subject to the MACT standard setting process in section 112(d) of the CAA. We delayed promulgating MACT standards for these source categories pending reevaluation of the MACT standard-setting methodology following the Court's decision to vacate the standards for the Phase I source categories. We also have entered into a judicially enforceable consent decree with Sierra Club that requires EPA to promulgate MACT standards for the Phase II sources by June 14, 2005, since extended to September 14, 2005—the same date that (for independent reasons) is required for the replacement standards for Phase I sources.
We proposed standards for HWCs on April 20, 2004 (69 FR 21197). The public comment period closed on July 6, 2004. In addition, on February 4, 2005, we requested certain key commenters to comment by email on a limited number of issues arising from public comments on the proposed rule. The comment period for those issues closed on March 7, 2005.
We received approximately 100 public comment letters on the proposed rule and the subsequent direct request for comments. Comments were submitted by owner/operators of HWCs, trade associations, state regulatory agencies and their representatives, and environmental groups. Today's final rule reflects our consideration of all of the comments and additional information we received. Major public comments on the proposed rule along with our responses, are summarized in this preamble.
The amendments to the Subpart EEE, Part 63, standards for hazardous waste combustors apply to the source categories that are currently subject to that subpart—incinerators, cement kilns, and lightweight aggregate kilns that burn hazardous waste. Today's final rule, however, also amends Subpart EEE to establish MACT standards for the Phase II source categories—those boilers and hydrochloric acid production furnaces that burn hazardous waste.
Generally speaking, you are an affected source pursuant to Subpart EEE if you combust, or have previously combusted, hazardous waste in an incinerator, cement kiln, lightweight aggregate kiln, boiler, or hydrochloric acid production furnace. You continue to be an affected source until you cease burning hazardous waste and initiate closure requirements pursuant to RCRA. Affected sources do not include: (1) Sources exempt from regulation under 40 CFR part 266, subpart H, because the only hazardous waste they burn is listed under 40 CFR 266.100(c); (2) research, development, and demonstration sources exempt under § 63.1200(b); and (3) boilers exempt from regulation under 40 CFR part 266, subpart H, because they meet the definition of small quantity burner under 40 CFR 266.108. See § 63.1200(b).
If you never previously combusted hazardous waste, or have ceased burning hazardous waste and initiated RCRA closure requirements, you are not subject to Subpart EEE. Rather, EPA has promulgated separate MACT standards for sources that do not burn hazardous waste within the following source categories: commercial and industrial solid waste incinerators (40 CFR Part 60, Subparts CCCC and DDDD); Portland cement manufacturing facilities (40 CFR Part 63, Subpart LLL); industrial/commercial/institutional boilers and process heaters (40 CFR Part 63, Subpart DDDDD); and hydrochloric acid production facilities (40 CFR Part 63, Subpart NNNNN). In addition, EPA considered whether to establish MACT standards for lightweight aggregate manufacturing facilities that do not burn hazardous waste, and determined that they are not major sources of HAP emissions. Thus, EPA has not established MACT standards for lightweight aggregate manufacturing facilities that do not burn hazardous waste.
Note that non-stack emissions points are not regulated under Subpart EEE.
Note that if you temporarily cease burning hazardous waste for any reason, you remain an affected source and are still subject to the applicable Subpart
Today's final rule protects air quality and promotes the public health by reducing the emissions of some of the HAP listed in Section 112(b)(1) of the CAA. Emissions data collected in the development of this final rule show that metals, hydrogen chloride and chlorine gas, dioxins and furans, and other organic compounds are emitted from hazardous waste combustors. The HAP that would be controlled with this rule are associated with a variety of adverse health affects. These adverse health effects include chronic health disorders (e.g., irritation of the lung, skin, and mucus membranes and effects on the blood, digestive tract, kidneys, and central nervous system), and acute health disorders (e.g., lung irritation and congestion, alimentary effects such as nausea and vomiting, and effects on the central nervous system). Provided below are brief descriptions of risks associated with HAP that are emitted from hazardous waste combustors.
Antimony occurs at very low levels in the environment, both in the soils and foods. Higher concentrations, however, are found at antimony processing sites, and in their hazardous wastes. The most common industrial use of antimony is as a fire retardant in the form of antimony trioxide. Chronic occupational exposure to antimony (generally antimony trioxide) is most commonly associated with “antimony pneumoconiosis,” a condition involving fibrosis and scarring of the lung tissues. Studies have shown that antimony accumulates in the lung and is retained for long periods of time. Effects are not limited to the lungs, however, and myocardial effects (effects on the heart muscle) and related effects (e.g., increased blood pressure, altered EKG readings) are among the best-characterized human health effects associated with antimony exposure. Reproductive effects (increased incidence of spontaneous abortions and higher rates of premature deliveries) have been observed in female workers exposed in an antimony processing facilities. Similar effects on the heart, lungs, and reproductive system have been observed in laboratory animals.
EPA assessed the carcinogenicity of antimony and found the evidence for carcinogenicity to be weak, with conflicting evidence from inhalation studies with laboratory animals, equivocal data from the occupational studies, negative results from studies of oral exposures in laboratory animals, and little evidence of mutagenicity or genotoxicity.
Chronic (long-term) inhalation exposure to inorganic arsenic in humans is associated with irritation of the skin and mucous membranes. Human data suggest a relationship between inhalation exposure of women working at or living near metal smelters and an increased risk of reproductive effects, such as spontaneous abortions. Inorganic arsenic exposure in humans by the inhalation route has been shown to be strongly associated with lung cancer, while ingestion or inorganic arsenic in humans has been linked to a form of skin cancer and also to bladder, liver, and lung cancer. EPA has classified inorganic arsenic as a Group A, human carcinogen.
Chronic inhalation exposure of humans to high levels of beryllium has been reported to cause chronic beryllium disease (berylliosis), in which granulomatous (noncancerous) lesions develop in the lung. Inhalation exposure to high levels of beryllium has been demonstrated to cause lung cancer in rats and monkeys. Human studies are limited, but suggest a causal relationship between beryllium exposure and an increased risk of lung cancer. We have classified beryllium as a Group B1, probable human carcinogen, when inhaled; data are inadequate to determine whether beryllium is carcinogenic when ingested.
Chronic inhalation or oral exposure to cadmium leads to a build-up of cadmium in the kidneys that can cause kidney disease. Cadmium has been shown to be a developmental toxicant in animals, resulting in fetal malformations and other effects, but no conclusive evidence exists in humans. An association between cadmium exposure and an increased risk of lung cancer has been reported from human studies, but these studies are inconclusive due to confounding factors. Animal studies have demonstrated an increase in lung cancer from long-term inhalation exposure to cadmium. EPA has classified cadmium as a Group B1, probable carcinogen.
Chlorine is an irritant to the eyes, the upper respiratory tract, and lungs. Chronic exposure to chlorine gas in workers has resulted in respiratory effects including eye and throat irritation and airflow obstruction. No information is available on the carcinogenic effects of chlorine in humans from inhalation exposure. A National Toxicology Program (NTP) study showed no evidence of carcinogenic activity in male rats or male and female mice, and equivocal evidence in female rats, from ingestion of chlorinated water. The EPA has not classified chlorine for potential carcinogenicity. In the absence of specific scientific evidence to the contrary, it is the Agency's policy to classify noncarcinogenic effects as threshold effects. RfC development is the default approach for threshold (or nonlinear) effects.
Chromium may be emitted in two forms, trivalent chromium (chromium III) or hexavalent chromium (chromium VI). The respiratory tract is the major target organ for chromium VI toxicity for inhalation exposures. Bronchitis, decreases pulmonary function, pneumonia, and other respiratory effects have been noted from chronic high does exposure in occupational settings due to chromium VI. Limited human studies suggest that chromium VI inhalation exposure may be associated with complications during pregnancy and childbirth, while animal studies have not reported reproductive effects from inhalation exposure to chromium VI. Human and animal studies have clearly established that inhaled chromium VI is
Chromium III is less toxic than chromium VI. The respiratory tract is also the major target organ for chromium III toxicity, similar to chromium VI. Chromium III is an essential element in humans, with a daily intake of 50 to 200 micrograms per day recommended for an adult. The body can detoxify some amount of chromium VI to chromium III. EPA has not classified chromium III with respect to carcinogenicity.
Cobalt is a relatively rare metal that is produced primarily as a by-product during refining of other metals, especially copper. Cobalt has been widely reported to cause respiratory effects in humans exposed by inhalation, including respiratory irritation, wheezing, asthma, and pneumonia. Cardiomyopathy (damage to the heart muscle) has also been reported, although this effect is better known from oral exposure. Other effects of oral exposure in humans are polycythemia (an abnormally high number of red blood cells) and the blocking of uptake of iodine by the thyroid. In addition, cobalt is a sensitizer in humans by any route of exposure. Sensitized individuals may react to inhalation of cobalt by developing asthma or to ingestion or dermal contact with cobalt by developing dermatitis. Cobalt is as a vital component of vitamin B
A number of epidemiological studies have found that exposures to cobalt are associated with an increased incidence of lung cancer in occupational settings. The International Agency for Research on Cancer (part of the World Health Organization) classifies cobalt and cobalt compounds as “possibly carcinogenic to humans” (Group 2B). The American Conference of Governmental Industrial Hygienists has classified cobalt as a confirmed animal carcinogen with unknown relevance to humans (category A3). An EPA assessment concludes that under EPA's cancer guidelines, cobalt would be considered likely to be carcinogenic to humans.
Exposures to 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TCDD) and related compounds at levels 10 times or less above those modeled to approximate average background exposure have resulted in adverse non-cancer health effects in animals. This statement is based on assumptions about the toxic equivalent for these compounds, for which there is acknowledged uncertainty. These effects include changes in hormone systems, alterations in fetal development, reduced reproductive capacity, and immunosuppression. Effects that may be linked to dioxin and furan exposures at low dose in humans include changes in markers of early development and hormone levels. Dioxin and furan exposures are associated with altered liver function and lipid metabolism changes in activity of various liver enzymes, depression of the immune system, and endocrine and nervous system effects. EPA in its 1985 dioxin assessment classified 2,3,7,8-TCDD as a probable human carcinogen. The International Agency for Research on Cancer (IARC) concluded in 1997 that the overall weight of the evidence was sufficient to characterize 2,3,7,8-TCDD as a known human carcinogen.
The chemical and environmental stability of dioxins and their tendency to accumulate in fat have resulted in their detection within many ecosystems. In the United States and elsewhere, accidental contamination of the environment by 2,3,7,8-TCDD has resulted in deaths in many species of wildlife and domestic animals.
Hydrogen chloride, also called hydrochloric acid, is corrosive to the eyes, skin, and mucous membranes. Chronic (long-term) occupational exposure to hydrochloric acid has been reported to cause gastritis, bronchitis, and dermatitis in workers. Prolonged exposure to low concentrations may also cause dental discoloration and erosion. No information is available on the reproductive or developmental effects of hydrochloric acid in humans. In rats exposed to hydrochloric acid by inhalation, altered estrus cycles have been reported in females and increased fetal mortality and decreased fetal weight have been reported in offspring. EPA has not classified hydrochloric acid for carcinogenicity. In the absence of specific scientific evidence to the contrary, it is the Agency's policy to classify noncarcinogenic effects as threshold effects. RfC development is the default approach for threshold (or nonlinear) effects.
Lead can cause a variety of effects at low dose levels. Chronic exposure to high levels of lead in humans results in effects on the blood, central nervous system, blood pressure, and kidneys. Children are particularly sensitive to the chronic effects of lead, with slowed cognitive development, reduced growth and other effects reported. Reproductive effects, such as decreased sperm count in men and spontaneous abortions in women, have been associated with lead exposure. The developing fetus is at particular risk from maternal lead exposure, with low birth weight and slowed postnatal neurobehavioral development noted. Human studies are inconclusive regarding lead exposure and cancer, while animal studies have reported an increase in kidney cancer from lead exposure by the oral route. EPA has classified lead as a Group B2, probable human carcinogen.
Health effects in humans have been associated with both deficiencies and excess intakes of manganese. Chronic exposure to low levels of manganese in the diet is considered to be nutritionally essential in humans, with a recommended daily allowance of 2 to 5 milligrams per day (mg/d). Chronic
Mercury exists in three forms: elemental mercury, inorganic mercury compounds (primarily mercuric chloride), and organic mercury compounds (primarily methyl mercury). Each form exhibits different health effects. Various sources may release elemental or inorganic mercury; environmental methyl mercury is typically formed by biological processes after mercury has precipitated from the air.
Chronic exposure to elemental mercury in humans also affects the central nervous system, with effects such as increased excitability, irritability, excessive shyness, and tremors. The EPA has not classified elemental mercury with respect to cancer.
The major effect from chronic exposure to inorganic mercury is kidney damage. Reproductive and developmental animal studies have reported effects such as alterations in testicular tissue, increased embryo resorption rates, and abnormalities of development. Mercuric chloride (an inorganic mercury compound) exposure has been shown to result in forestomach, thyroid, and renal tumors in experimental animals. EPA has classified mercuric chloride as a Group C, possible human carcinogen.
Nickel is an essential element in some animal species, and it has been suggested it may be essential for human nutrition. Nickel dermatitis, consisting of itching of the fingers, hand and forearms, is the most common effect in humans from chronic exposure to nickel. Respiratory effects have also been reported in humans from inhalation exposure to nickel. No information is available regarding the reproductive of developmental effects of nickel in humans, but animal studies have reported such effects, although a consistent dose-response relationship has not been seen. Nickel forms released from industrial boilers include soluble nickel compounds, nickel subsulfide, and nickel carbonyl. Human and animal studies have reported an increased risk of lung and nasal cancers from exposure to nickel refinery dusts and nickel subsulfide. Animal studies of soluble nickel compounds i.e., nickel carbonyl) have reported lung tumors. The EPA has classified nickel refinery subsulfide as a Group A, human carcinogen and nickel carbonyl as a Group B2, probable human carcinogen.
Organic HAPs include halogenated and nonhalogenated organic classes of compounds such as polycyclic aromatic hydrocarbons (PAHs) and polychlorinated biphenyls (PCBs). Both PAHs and PCBs are classified as potential human carcinogens, and are considered toxic, persistent and bioaccumulative. Organic HAP also include compounds such as benzene, methane, propane, chlorinated alkanes and alkenes, phenols and chlorinated aromatics. Adverse health effects of HAPs include damage to the immune system, as well as neurological, reproductive, developmental, respiratory and other health problems.
Atmospheric particulate matter (PM) is composed of sulfate, nitrate, ammonium, and other ions, elemental carbon, particle-bound water, a wide variety of organic compounds, and a large number of elements contained in various compounds, some of which originate from crustal materials and others from combustion sources. Combustion sources are the primary origin of trace metals found in fine particles in the atmosphere. Ambient PM can be of primary or secondary origin.
Exposure to particles can lead to a variety of serious health effects. The largest particles do not get very far into the lungs, so they tend to cause fewer harmful health effects. Fine particles pose the greatest problems because they can get deep into the lungs. Scientific studies show links between these small particles and numerous adverse health effects. Epidemiological studies have shown a significant correlation between elevated PM levels and premature mortality. Other important effects associated with PM exposure include aggravation of respiratory and cardiovascular disease (as indicated by increased hospital admissions, emergency room visits, absences from school or work, and restricted activity days), lung disease, decreased lung function, asthma attacks, and certain cardiovascular problems. Individuals particularly sensitive to PM exposure include older adults and people with heart and lung disease.
This is only a partial summary of adverse health and environmental effects associated with exposure to PM. Further information is found in the 2004 Criteria Document for PM (“Air Quality Criteria for Particulate Matter,” EPA/600/P-99/002bF) and the 2005 Staff Paper for PM (EPA, “Review of the National Ambient Air Quality Standards for Particulate Matter, Policy Assessment of Scientific and Technical Information: OAQPS Staff Paper,” (June 2005)).
Selenium is a naturally occurring substance that is toxic at high concentrations but is also a nutritionally essential element. Studies of humans chronically exposed to high levels of selenium in food and water have reported discoloration of the skin, pathological deformation and loss of nails, loss of hair, excessive tooth decay and discoloration, lack of mental alertness, and listlessness. The consumption of high levels of selenium by pigs, sheep, and cattle has been shown to interfere with normal fetal development and to produce birth defects. Results of human and animal studies suggest that supplementation with some forms of selenium may result in a reduced incidence of several tumor types. One selenium compound, selenium sulfide, is carcinogenic in animals exposed orally. We have classified elemental selenium as a Group D, not classifiable as to human carcinogenicity, and selenium sulfide as a Group B2, probable human carcinogen.
Today's rule promulgates standards for controlling emissions of HAP from hazardous waste combustors: incinerators, cement kilns, lightweight aggregate kilns, boilers, and hydrochloric acid production furnaces that burn hazardous waste. A description of each source category can be found in the proposed rule (see 69 FR at 21207-08).
Hazardous waste burning incinerators, cement kilns, and lightweight aggregate kilns are currently subject to 40 CFR part 63, subpart EEE, National Emission Standards for Hazardous Air Pollutants (NESHAP). Today's rule revises the emissions limits and certain compliance and monitoring provisions of subpart EEE for these
Boilers that burn hazardous waste are also affected sources under today's rule. The rule uses the RCRA definition of a boiler under 40 CFR 260.10 and includes industrial, commercial, and institutional boilers as well as thermal units known as process heaters. Hazardous waste burning boilers will continue to comply with the emission standards found under 40 CFR part 266, subpart H (i.e., the existing RCRA rules) until they demonstrate compliance with the requirements of 40 CFR part 63, subpart EEE, and, for permitted sources, subsequently remove these requirements from their RCRA permit.
Finally, hydrochloric acid production furnaces that burn hazardous waste are affected sources under today's rule. These furnaces are a type of halogen acid furnace included in the definition of “industrial furnace” defined at § 260.10. Hydrochloric acid production furnaces that burn hazardous waste will continue to comply with the emission standards found under 40 CFR part 266, subpart H, until they demonstrate compliance with 40 CFR part 63, subpart EEE, and, for permitted sources, subsequently remove these requirements from their RCRA permit.
Today's rule apply to each major and area source incinerator, cement kiln, lightweight aggregate kiln, boiler, and hydrochloric acid production furnace that burns hazardous waste.
Hazardous waste combustors emit dioxin/furans, sometimes at high levels depending on the design and operation of the emission control equipment, and, for incinerators, depending on whether a waste heat recovery boiler is used. All hazardous waste combustors can also emit high levels of other organic HAP if they are not designed, operated, and maintained to operate under good combustion conditions.
Hazardous waste combustors can also emit high levels of metal HAP, depending on the level of metals in the waste feed and the design and operation of air emissions control equipment. Hazardous waste burning hydrochloric acid production furnaces, however, generally feed and emit low levels of metal HAP.
All of these HAP metals (except for the volatile metal mercury) are emitted as a portion of the particulate matter emitted by these sources. Hazardous waste combustors can also emit high levels of particulate matter, except that hydrochloric acid production furnaces generally feed hazardous wastes with low ash content and consequently emit low levels of particulate matter. A majority of particulate matter emissions from hazardous waste combustors are in the form of fine particulate. Particulate emissions from incinerators and liquid fuel-fired boilers depend on the ash content of the hazardous waste feed and the design and operation of air emission control equipment. Particulate emissions from cement kilns and lightweight aggregate kilns are not significantly affected by the ash content of the hazardous waste fuel because uncontrolled particulate emissions are attributable primarily to fine raw material entrained in the combustion gas. Thus, particulate emissions from kilns depends on operating conditions that effect entrainment of raw material, and the design and operation of the emission control equipment.
The final rule applies to you if you own or operate a hazardous waste combustor—an incinerator, cement kiln, lightweight aggregate kiln, boiler, or hydrochloric acid production facility that burns hazardous waste. The final rule does not apply to a source that meets the applicability requirements of § 63.1200(b) for reasons explained at 69 FR at 21212-13.
You must meet the emission limits in Tables 1 and 2 of this preamble for your applicable source category and subcategory. Standards are corrected to 7 percent oxygen. As noted at proposal, we previously promulgated requirements for carbon monoxide, total hydrocarbon, and destruction and removal efficiency standards under subpart EEE for incinerators, cement kilns, and lightweight aggregate kilns. We view these standards as unaffected by the Court's vacature of the challenged regulations in its decision of July 24, 2001. We are therefore not re-promulgating and reopening consideration of these standards in today's final rule, but are summarizing these standards in Tables 1 and 2 for reader's convenience.
Liquid fuel boilers equipped with dry air pollution control devices are subject to different dioxin/furan emission standards than liquid fuel boilers that are not equipped with dry air pollution control devices.
For any of the source categories except hydrochloric acid production
Incinerators and liquid and solid fuel boilers may elect to comply with an alternative to the particulate matter standard that would limit emissions of all the semivolatile metal HAPs and low volatile metal HAPs. Under this alternative, the numerical emission limits for semivolatile metal and low volatile metal emission HAP are identical to the limitations included in Tables 1 and 2. However, for semivolatile metals, the alternative standard applies to the combined emissions of lead, cadmium, and selenium; for low volatile metals, the standard applies to the combined emissions of chromium, arsenic, beryllium, antimony, cobalt, manganese, and nickel. See § 63.1219(e).