Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 1 Final Draft Chapter VII. Mechanism of Toxicity and Sensitive Subpopulations A. Biochemical Basis of Toxicity Both DBAN and DCAN are general systemic toxicants, with depressed body weight identified as a common adverse effect ( NTP, 2002; Hayes et al., 1996). Although other organ weight changes were observed at doses associated with decreased body weight, the liver is an organ for which dose dependent effects on organ weight were supported by other measures of toxicity. Increased enzyme levels ( e. g., ALP) in the serum were observed at doses higher than those that induced liver weight changes ( Hayes et al., 1986), suggesting that DBAN and DCAN might induce hepatocellular necrosis. However, ALP is not a liver specific enzyme, and changes in the liver specific enzymes SGPT and SGOT were not consistently dose related. In addition,

Hayes et al. ( 1986) did not perform histopathological examinations, and therefore, cellular changes resulting in increased liver weight could not be determined. The data suggest that DCAN may be the more potent liver toxicant compared to DBAN, since the observed effects in the gavage study ( Hayes et al., 1986) for DCAN were more severe than for DBAN. Furthermore,

DBAN administered in drinking water did not induce liver toxicity, other than a treatment related increase in liver GST activity ( NTP, 2002). However, the highest doses in the drinking water study ( NTP, 2002) were similar to the NOAEL in the Hayes et al. ( 1986) study. None of the available data are adequate to determine mechanisms of liver toxicity for the HANs.

One postulated mode of action for the toxicity of haloacetonitriles ( HANs) is through direct interactions with cellular macromolecules ( Pereira et al., 1984; Daniel et al., 1986; Lin and Guion, 1989; Lin et al., 1992). Depletion of reduced glutathione ( GSH) could also play a role. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 2 Final Draft HANs have been shown to induce transient decreases in rat liver GSH levels and inhibit glutathione S transferase activity in vivo ( Lin and Guion, 1989; Ahmed et al., 1991). Ahmed et al. ( 1989) noted that the relative degree of inhibition of rat liver glutathione S transferase ( GST)

activity in vitro, reported as TCAN> DBAN> DCAN, is consistent with the relative toxicity of these compounds reported in the literature, suggesting perturbation of GSH protection as an important mechanism of toxicity. As further support for the relatedness of GSH depletion and HAN induced toxicity, Ahmed et al. ( 1991) noted that the sustained depletion of cellular GSH levels in stomach tissues by DBAN was consistent with their earlier preliminary finding that acute oral doses of HANs can damage the gastric tissues. However, the effect of HANs on gastric tissue might simply reflect the direct irritancy of these compounds, rather than GSH depletion.

The initial finding of HANs damaging gastric tissues cannot be further investigated, because the subacute and subchronic studies ( Hayes et al., 1986) did not include a histopathological examination of the stomach.

GSH depletion could enhance cytotoxicity by allowing damage to cellular macromolecules by HANs, their metabolites, or other reactive species accumulated in the cell. Since GSH is an important cellular antioxidant, its depletion might induce cellular oxidative stress. In support of this idea, Ahmed et al. ( 1999) reported that orally administered monochloroacetonitrile ( MCAN)

induced a dose dependent decrease in GSH levels and increased levels of oxidative DNA damage in the stomach mucosa of rats. Alternative mechanisms for MCAN induced oxidative stress were discussed by the study authors. One proposed mechanism involves GSH depletion, resulting in decreased ability of the cell to detoxify endogenous reactive oxygen species. In an alternative mechanism, cyanide derived from MCAN metabolism might alter cellular oxygen utilization and Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 3 Final Draft increase the formation of reactive oxygen species. In agreement with the proposed role of oxidative stress, Mohamadin and Abdel Naim ( 1999) reported that MCAN decreased cellular GSH content and increased lipid peroxidation, as measured by the concentration of thiobarbituric acid reactive substances ( TBARS), in rat gastric epithelial cells in culture. Cell viability, measured by the release of lactate dehydrogenase activity, was correlated with the depletion of cellular GSH levels ® = 0.96). Supplementing the culture medium with treatments that protect against cellular oxidative stress ( e. g. antioxidants or iron chelators), decreased the cytotoxicity and lipid peroxidation induced by MCAN. MCAN is not a compound under review for this document.

However, since it shares the ability to deplete GSH and form cyanide with other HANs, these data are appropriate for discussion here, although in generalizing about the HANs as a class of compounds, differences in their ability to deplete GSH should be considered in evaluating the likely mechanisms for any individual compound.

In addition to the induction of oxidative stress secondary to GSH depletion or cyanide activity on cell respiration, an alternative pathway might include activation of macrophages to release reactive oxygen species. Ahmed et al. ( 2000) reported that DCAN induced oxidative stress responses, including increased oxidation of glutathione, increased formation of reactive oxygen intermediates, and increased tumor necrosis factor alpha ( TNF  ) secretion ( a cellular response during macrophage activation) in a mouse macrophage cell line in culture. To explain these data, the authors proposed that DCAN treatment activates macrophages, with subsequent increases in reactive oxygen intermediate production and in TNF   secretion. The increased production of reactive oxygen species induces oxidative stress that reduces cell viability through apoptosis and necrosis. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 4 Final Draft The identification of thiocyanate as a urinary metabolite in animals orally dosed with HANs, and the hypothesized metabolism to cyanide ( Pereira et al., 1984), suggest additional possible effects of HANs that should be investigated. Longer term exposure to thiocyanate ( either from thiocyanate dosing or as a metabolite of cyanide) causes thyroid effects. Central nervous system effects ( e. g., myelin degeneration) and male reproductive effects ( decreased epididymal weight and sperm motility) have also been observed following long term exposure to cyanide ( U. S. EPA, 2002c). Effects on the central nervous system or thyroid were not observed in a recent 14 day or 13 week NTP ( 2002) study for DBAN. Although decreased testes weight and testes atrophy were reported in the 14 day ( NTP, 2002) study for DBAN, this effect has not been observed in subchronic studies ( Hayes et al., 1986; NTP, 2002), or in other studies that evaluated male reproductive tract parameters ( R. O. W. Sciences, 1997; Meier et al., 1985).

However, only limited conclusions can drawn regarding the potential for HANs to induce a similar array of effects as cyanide and thiocyanate, based on limitations in the overall database.

A comparison of relative potency among HANs in thiocyanate excretion, alkylation potential ( p nitrobenzopyridine binding), protein binding ( inhibition of dinitrosamine demethylase activity), and production of DNA strand breaks, suggested that relative thiocyanate excretion did not correspond well to some of these markers of potential macromolecule interaction ( Pereira et al., 1984). For example, monochloroacetonitrile ( MCAN) was the most potent thiocyanate former, but TCAN was more potent than MCAN in protein binding and inducing DNA strand breaks. The authors suggested that this discordance between propensity for cyanide formation and induction of toxic outcomes might reflect the formation of reactive intermediates other than cyanide from TCAN, such as phosgene and cyanoformyl chloride. The results of the comparative Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 5 Final Draft analysis by Pereira et al. ( 1984) suggest that intermediate metabolites, other than cyanide, may be important in producing some of the toxic effects observed for HANs. In further support of this conclusion, the systemic toxicity induced by cyanide and thiocyanate does not closely parallel the range of effects observed for HANs. For example, cyanide and thiocyanate are not potent liver toxicants, a target organ for the effects of HANs ( U. S. EPA, 2002c).

BCAN, DBAN, DCAN, and TCAN all cause developmental toxicity in vivo ( Smith et al.,

1986; Smith et al., 1987; Smith et al., 1988; Smith et al., 1989; Christ et al., 1995; Christ et al.,

1996), but the relative potency of these compounds is unclear, due to the likely potentiating effects of the solvent vehicle ( tricaprylin) used in these studies ( Christ et al., 1996).

As discussed in Chapter III ( Toxicokinetics), it remains unclear whether the potentiating effect of tricaprylin on the developmental toxicity of HANs represents a toxicokinetic or toxicodynamic interaction, or whether both of these mechanisms play a role. Since the data on tricaprylin effects for HANs were limited to two published abstracts ( Roth et al., 1990; Gordon et al., 1991), a review of the literature on interactions between solvent vehicles and other disinfectant by products or unsaturated nitriles was done to determine whether a consistent relationship could be found. Solvent vehicles are needed for studies with these compounds, due to the minimal water solubility. No data were found for interactions between tricaprylin and the comparison compounds. Therefore, data on observed solvent vehicle interactions are too limited for trihalomethanes and unsaturated nitriles to be useful in reaching a general conclusion about the mechanisms involved in the ability of tricaprylin to potentiate the developmental toxicity of HANs. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 6 Final Draft Developmental toxicity has been observed even in the absence of confounding by tricaprylin, at least for TCAN ( Christ et al., 1996). Maternal toxicity was observed at lower doses than developmental effects in this study, and therefore, it is possible that the observed developmental effects were secondary to maternal effects. Mechanistic explanations for the developmental toxicity of HANs have been explored, including cyanide formation and glutathione depletion. Early evidence suggested that the developmental toxicity of HANs might not be secondary to cyanide formation. When a maximally tolerated dose of a series of HANs in a tricaprylin vehicle was administered to Long Evans rats, developmental toxicity was greatest for the highly chlorine substituted acetonitriles ( Smith et al., 1986). These results were contrasted with the work of Pereira et al. ( 1984), who found that thiocyanate excretion ( and hence cyanide production) is inversely related to chlorine substitution. Based on this comparison, in which greater chlorine substitution increases developmental toxicity and decreases thiocyanate excretion,

the authors concluded that the degree of developmental toxicity was not due to cyanide formation. However, conclusions drawn from the HANs studies must be tempered by uncertainty regarding their true relative developmental toxicity potencies. The tricaprylin vehicle used in the developmental toxicity studies causes developmental effects by itself ( Smith et al., 1989; Christ et al., 1995), and interacts with TCAN to cause both qualitative changes in the spectrum of developmental effects, as well as more than additive quantitative changes. Because of these effects of the vehicle used in the relevant developmental toxicity studies, and because the relative potentiating ability of tricaprylin may differ for each of the HANs tested, the true relative developmental toxicity potencies are unknown. Another potential avenue for determining the contribution of cyanide to the developmental toxicity of HANs would be to compare the developmental effects observed in animals exposed to cyanide versus those observed for HANs. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 7 Final Draft However, the available developmental toxicity studies for both HANs ( see Chapter V) and cyanide ( U. S. EPA, 2002c) are too limited to conduct a meaningful comparison of their relative potencies as developmental toxicants.

Christ et al. ( 1995), in a study on the developmental toxicity of BCAN, reiterated the discordance between developmental toxicity and degree of metabolism to cyanide, and introduced GSH depletion as another possible mechanism for developmental toxicity. To address the role of GSH depletion in the developmental toxicity of HANs, Christ et al. ( 1995) cited the study of Abdel Aziz et al. ( 1993), who compared maternal and fetal uptake of [ 2 14C] MCAN in CD 1 mice. Abdel Aziz et al. ( 1993) treated dams with diethylmaleate ( DEM) by intraperitoneal injection to induce an oxidative stress response on gestation day 13. One hour later, control mice and DEM pretreated mice were given a 77 mg/ kg dose of radiolabeled MCAN by i. v. injection.

MCAN treatment significantly decreased maternal liver, uterus, and fetal tissue levels of GSH,

and the degree of GSH depletion was further increased in the DEM pretreated mice. Urinary excretion of thiocyanate, a measure of MCAN metabolism, was five times higher in the DEMpretreated mice given MCAN as compared to control mice treated with MCAN only. MCAN equivalents determined from the yield of radioactivity in maternal uterine tissues, amniotic fluid,

and in fetuses rose rapidly to similar levels at 1 hour for both DEM pretreated mice and mice not given DEM. In the absence of DEM pretreatment, MCAN equivalents declined rapidly for all three tissues examined. However, in DEM pretreated animals, the removal of tissue radioactivity was significantly slower. At 24 hours, the level of MCAN equivalents was two fold higher in fetal DNA than in maternal uterine DNA. This effect was further enhanced by DEM pretreatment.

The total DNA bound MCAN equivalent level in DEM pretreated mice was four fold higher in Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 8 Final Draft fetal DNA than in maternal uterine DNA, suggesting that fetuses might be particularly sensitive to the effects of GSH depletion. Based on the increases in thiocyanate excretion and DNA binding under oxidative stress conditions that deplete GSH, the authors suggested that GSH depletion increases the metabolism of the remaining unconjugated MCAN and/ or increases the availability of MCAN to react directly with cellular macromolecules such as DNA. These data suggest that the developmental toxicity of HANs may be directly related to the ability of these compounds to deplete GSH levels.

Saillenfait and Sabate ( 2000) tested the developmental toxicity of aliphatic nitriles ( sodium cyanide, acetonitrile, propionitrile, n butyronitrile, acrylonitrile, methacrylonitrile, allylnitrile, cis

2 pentenenitrile, and 2 chloroacrylonitrile) in a rat whole embryo assay and in vivo. Although no HANs were included in this study, the results may have implications for the developmental toxicity of HANs based on similar chemical reactivity. In the whole embryo testing experiment, a wide range of embryotoxicity was observed. In addition, no common pattern of developmental effects was observed among all the compounds tested. Enhancement of metabolism by supplementation of the cultures with microsomes increased the severity of embryolethality and developmental toxicity for the unsaturated aliphatic nitriles ( e. g., acrylonitrile), but not the saturated aliphatic nitriles ( e. g., acetonitrile). This result, coupled with the difference between the spectrum of dysmorphogenesis observed for the unsaturated nitriles and for embryos treated with sodium cyanide, led the authors to suggest that microsomal metabolism of unsaturated nitriles generates toxic metabolites in addition to cyanide. In further support of a mechanism distinct from cyanide release for the in vitro developmental toxicity of the tested compounds, their relative Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 9 Final Draft potency in the whole embryo culture assay did not directly correspond with increasing cyanide release kinetics as determined from in vitro metabolism studies.

No haloacetontriles were included in the study by Saillenfait and Sabate ( 2000), but based on their shared ability to deplete cellular GSH ( as described in the rest of this paragraph), HANs may act chemically more like unsaturated nitriles than saturated ones, and thus may induce developmental toxicity through mechanisms other than cyanide release. Ahmed et al. ( 1982)

reported that unsaturated but not saturated aliphatic nitriles decrease liver glutathione levels.

Clinical signs of toxicity were different for unsaturated nitriles than for potassium cyanide, while animals administered saturated nitriles and potassium cyanide showed a similar spectrum of symptoms. Taken together, the results of Saillenfait and Sabate ( 2000) and Ahmed et al. ( 1982)

suggest that reactive metabolites in addition to cyanide might be important for the induction of developmental toxicity. In further support for a common toxic mechanism for unsaturated nitriles and HANs, Smith et al. ( 1989) noted that a similar spectrum of soft tissue malformations is observed for TCAN, DCAN, and the unsaturated nitrile, acrylonitrile. However, later evidence presented by Christ et al. ( 1996), demonstrated that the use of tricaprylin in these earlier studies might have caused a shift in the type of soft tissue malformations, placing the earlier conclusion in doubt.

Some results, however, do suggest an involvement of cyanide in the developmental toxicity of HANs. In contrast to their whole embryo assay results, Saillenfait and Sabate ( 2000)

reported similarities in the spectrum of developmental effects induced by all of the nitriles when tested in vivo. In this experiment, CD 1 mice dams received a single dose of aliphatic nitrile on Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 10 Final Draft gestation day 10, and evaluation of embryos for defects was conducted on gestation day 12. The dysmorphogenic effects characteristic of sodium cyanide, including misdirected allantois ( a tubular structure of the embryonic hindgut), trunk, or caudal extremity were induced by saturated as well as unsaturated aliphatic nitriles. The concordance in these results in vivo is consistent with cyanide being an active moiety for both saturated and unsaturated aliphatic nitriles.

Moudgal et al. ( 2000) evaluated relationships between the structure of 244 disinfectant byproducts, including 21 nitriles, and potential developmental toxicity using a rat oral developmental toxicity submodel of TOPKAT ® , a quantitative structure toxicity relationship ( QSTR) prediction tool. Based on individual structural descriptors, model probabilities were used to derive qualitative estimates as follows: 0.0 to 0.3 negative, 0.3 to 0.7 indeterminate, 0.7 to 1.0 positive. The probability estimate is independent of the potency or severity of developmental effects that could be induced, and would be interpreted as the likelihood that the chemical can cause developmental toxicity in rats following oral dosing. As a group, the nitrile disinfectant byproducts were characterized as having a high probability of developmental toxicity. Of the 21 individual nitrile compounds, 13 were positive, 5 were negative, and for 3 the model did not make a prediction. Only three of the four specific HANs under consideration in this document were assessed. DBAN and TCAN were predicted as positive and BCAN was predicted as negative.

TCAN was one of the chemicals in the model training set. Four other HANs were predicted as positive. A cursory evaluation of these data do not reveal a clear reason for the negative prediction for BCAN, since positive results were obtained for bromoacetonitrile,

bromodichloroacetonitrile, and dibromochloroacetonitrile. The effects of individual structural moieties were also examined by the software for various structural classes of compounds. The Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 11 Final Draft nitrile moiety, chlorine atom, and bromine atom were identified as contributing most significantly to the developmental toxicity predictions for the group of 20 nitriles. The importance of the nitrile group in the developmental toxicity predictions is consistent with cyanide as a causal factor in the developmental toxicity of these compounds in vivo, since this functional group gives rise to cyanide during HAN metabolism.

In summary, mechanisms of toxicity for noncarcinogenic effects ( decreased body weight,

gastric and liver toxicity, and developmental effects) have been hypothesized to be related to direct interaction with cellular proteins ( disrupting critical enzyme functions), depletion of cellular antioxidant defenses ( i. e, depletion of GSH and inhibition of GST), or effects secondary to cyanide formation. The data are not adequate to rule out any of these possibilities, and therefore,

any or all of these mechanisms could be involved.

B. Mechanism of Carcinogenesis The carcinogenic potential of the HANs is unknown. No epidemiological studies have evaluated directly the carcinogenic potential of HANs in humans. Rather, studies have evaluated the carcinogenic potential of chlorinated versus unchlorinated drinking water or the presence of trihalomethanes as a marker of chlorination by products ( IARC, 1999; Mills et al., 1998). Many of these studies have shown an association between chronic exposure to chlorinated water and increased risks of bladder, rectal, or colon cancers ( Mills et al., 1998; WHO, 2000). No standard cancer bioassays of HANs have been done in animals. Limited short term exposure data from the mouse skin assay ( Bull et al., 1985) and the mouse lung assay ( Bull and Robinson, 1985) indicate that BCAN, DBAN, and TCAN may be tumorigenic, although DBAN, DCAN, and TCAN were Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 12 Final Draft reported to be negative in the rat liver GGT foci assay ( Herren Freund and Pereira, 1986). In a qualitative review of structure activity relationships, Bull and Robinson ( 1985) discussed potential structural relationships among the results for the cancer screening assays and genotoxicity results for various HANs. They commented that there is no apparent consistent pattern in the potency of the individual compounds across the various assays.

Quantitative analysis of structural relationships of HANs with carcinogenic outcomes have also been investigated. Moudgal et al. ( 2000) evaluated relationships between the structure of 244 disinfectant byproducts, including 21 HANs, and potential carcinogenicity using mouse and rat oral submodels of TOPKAT ® , a quantitative structure toxicity relationship ( QSTR) prediction tool. As a group, the nitrile disinfectant byproducts were characterized as having a low probability of carcinogenicity. However, for the subset of six HANs in the total group of 20 nitrile compounds for which individual data were presented ( carcinogenicity predictions for TCAN were not included), four were predicted as positive in at least one sex in mice or rats. The results were largely mixed across species or sex for each test compound. For example, BCAN was predicted as positive in male and female mice, but negative in both sexes of rats. DBAN was negative in both sexes of mice, and female rats, but indeterminate in male rats. These QSTR results are consistent with the screening bioassays in indicating at least limited carcinogenic potential of the HANs.

The HANs or their metabolites are reactive compounds that can bind macromolecules including DNA ( Daniel et al., 1986; Lin et al., 1992). Nouraldeen and Ahmed ( 1996)

demonstrated in vitro that the degree of DNA binding was much lower for DCAN and TCAN Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 13 Final Draft than it was for bromoacetonitrile or MCAN. Based on changes in fluorescence as a measure of adduct formation, relative DNA adduct formation as compared to bromoacetonitrile was 8.6%,

1.0%, and 0.2% for MCAN, DCAN, and TCAN respectively. The chemical nature of the adducts that were formed was not identified for each compound. However, a 7

( cyanomethyl) guanine adduct was the single major adduct identified from the reaction of bromoacetonitrile with calf thymus DNA. Since the more fully halogenated acetonitriles BCAN,

DBAN, DCAN, and TCAN, may be metabolized to monohaloacetonitriles in vivo ( Pereira et al.,

1984), they might induce the formation of similar adducts. On the other hand, the relative DNA reactivity observed in vitro may not directly translate to mutagenic or carcinogenic potential in vivo, since the metabolism of the compound and the mutagenicity of the adducts formed may differ for each HAN.

Glutathione conjugation may be an important cellular protection against these reactive HANs or their metabolites ( Lin and Guion, 1989; Ahmed et al., 1991). The genotoxicity of each of the HAN compounds BCAN, DBAN, DCAN, and TCAN has been evaluated in at least one assay, and in most cases a variety of different assays. Although some of the data have provided contradictory results, all of the tested compounds appear to have some capacity to induce genotoxic effects. For example, BCAN, DCAN, and TCAN ( but not DBAN) have been found to generate a positive result in at least one reported Salmonella/ microsome assay. In addition, while not uniformly consistent, a variety of other assays, including those for chromosome effects, have yielded positive results for some of the HANs. Overall, these data suggest that HANs induce genotoxicity through direct interactions with DNA. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 14 Final Draft C. Interactions and Susceptibilities Potential Interactions No studies on interactions of HANs with other classes of compounds were identified,

except as noted above for solvent vehicle effects.

Childhood Susceptibility As discussed above, developmental toxicity has been associated with exposure to BCAN,

DBAN, DCAN, and TCAN, although the findings for all these compounds, except TCAN, are confounded by the developmental toxicity of the vehicle. The developmental toxicity of the HANs is supported by the reports of Roth et al. ( 1990) and Gordon et al. ( 1991) in published abstracts that radioactivity was detected in embryos of dams given [ 14C] TCAN, suggesting that fetuses may be targets for HAN toxicity. In addition, Abdel Aziz et al. ( 1993) found that fetuses may be more susceptible than adults to direct DNA damage induced by haloacetontriles.

Although the relationship between metabolism of HANs and the onset of toxicity has not been thoroughly determined ( as discussed above), acute cyanide intoxication from accidental pediatric acetonitrile exposures ( Caravati et al., 1988; Geller et al., 1991; Kurt et al., 1991) indicates that HAN metabolism to cyanide occurs in children.

There are limited data available for assessing directly the susceptibility of fetuses and children to HANs. No systemic toxicity studies have been identified that evaluated age related Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 15 Final Draft differences in sensitivity and no multigeneration reproductive studies have been reported. In addition, age related differences in the metabolism of the HANs could not be investigated,

because the enzyme( s) responsible for HAN metabolism are not known. Pereira et al. ( 1984)

hypothesized that mixed function oxidases are involved, but the isozyme involved has not been identified, and the age dependent expression differs among the different cytochrome P450 isozymes. Although the developmental toxicity of the HANs has been evaluated, most of the available literature cannot be used to determine relative maternal and developmental toxicity of these compounds, due to potential interactions between the test compound and the dosing vehicle ( tricaprylin). Excluding these studies from this evaluation leaves only limited data. No developmental toxicity was observed following administration of up to 10.9 mg/ kg/ day DBAN in drinking water ( R. O. W. Sciences, 1997), but this was only a screening study that did not include evaluation of pups for malformations. The only maternal effect at this dose was a decrease in drinking water consumption. In a study using corn oil as the solvent vehicle for TCAN, the maternal NOAEL was 15 mg/ kg/ day and the NOAEL for developmental toxicity was 35 mg/ kg/ day ( Christ et al., 1996). Thus, these two studies do not provide evidence that fetuses are more susceptible than adults, although the data are too limited to make a definitive conclusion.

Other potential susceptibilities Although a role of oxidative metabolism and glutathione conjugation have been hypothesized to be involved in HAN metabolism, the identity of enzymes involved in these pathways has not been determined. Therefore, the potential role of interindividual differences in metabolism due to genetic polymorphism, age, or other factors cannot be determined. Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 16 Final Draft D. Summary The HANs induce general systemic toxicity. Decreased body weight and a variety of organ weight changes occur following oral dosing, and the testes ( NTP, 2002) and liver might be particularly sensitive ( Hayes et al., 1986), although the reported effects in these organs in available studies are fairly limited. The HANs also induce developmental effects ( Smith et al.,

1986; Smith et al., 1987; Smith et al., 1988; Smith et al., 1989; Christ et al., 1995; Christ et al.,

1996). The mechanism( s) of toxicity are not known, but several possibilities have been described.

HANs may act through direct interactions with cellular macromolecules such as DNA ( Daniel et al., 1986; Lin et al., 1992; Nouraldeen and Ahmed, 1996). HAN toxicity might be secondary to GSH depletion ( Ahmed et al., 1991) or oxidative stress ( Ahmed et al., 1999; Mohamadin and Abdel Naim, 1999). Formation of cyanide from HAN might be another important mechanism of toxicity, although important systemic effects that are sensitive indicators of cyanide toxicity have not been fully examined.

The role of cyanide in the developmental toxicity of HANs has received much attention.

Some studies suggest that metabolites other than cyanide play a critical role ( Smith et al., 1986),

and implicated glutathione depletion as an important factor ( Christ et al., 1995; Abdel Aziz et al.,

1993). Although some indirect data supports a role of cyanide ( Moudgal et al., 2000; Saillenfait and Sabate, 2000), evaluation of the available developmental toxicity studies of cyanide itself do not support this hypothesis ( U. S. EPA, 2002c).

The ability of the HANs to bind to cellular macromolecules ( Daniel et al., 1986; Lin et al.,

1992; Nouraldeen and Ahmed, 1996), as well as generally positive results in genotoxicity assays, Drinking Water Criteria Document for Haloacetonitriles EPA/ OW/ OST/ HECD VII 17 Final Draft supports direct DNA damage as the mode of action for the tumorigenicity observed in cancer screening studies ( Bull et al., 1985; Bull and Robinson, 1985). However, the carcinogenic potential of the HANs is unknown, since epidemiology studies are not available and standard cancer animal bioassays of HANs have not been conducted.

Identification of potential susceptible subpopulations is hampered by the incomplete characterization of HAN metabolism or identification of the toxic moiety. Although a metabolic pathway for the HANs has been proposed ( Pereira et al., 1984), the enzymes important for catalyzing HAN metabolism are unknown. In addition, no studies on age dependent differences in metabolism or toxicity were identified, although one study demonstrated that HANs may bind more greatly to fetal DNA than to DNA in maternal tissues ( Abdel Aziz et al., 1993). Analysis of the developmental toxicity studies for TCAN revealed a lower maternal than developmental NOAEL, which does not suggest that fetuses are more susceptible than adults.


[Federal Register Volume 81, Number 47 (Thursday, March 10, 2016)]
[Proposed Rules]
[Pages 12637-12641]
[FR Doc No: 2016-05278]

-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R09-OAR-2015-0819; FRL-9943-47-Region 9]

Revisions to the California State Implementation Plan; South
Coast Air Quality Management District; Control of Oxides of Nitrogen
Emissions From Off-Road Diesel Vehicles

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

-----------------------------------------------------------------------

SUMMARY: The Environmental Protection Agency (EPA) is proposing to
approve South Coast Air Quality Management District's (SCAQMD or
District) Rule 2449, Control of Oxides of Nitrogen Emissions from Off-
Road Diesel Vehicles, which adopts by reference title 13, chapter 9,
section 2449.2 of the California Code of Regulations (CCR), ``Surplus
Off-Road Opt-In for NOX (SOON) Program,'' as part of the
SCAQMD portion of the California State Implementation Plan (SIP).
SCAQMD Rule 2449 requires certain in-use off-road vehicle fleets to
meet more stringent requirements in the South Coast area when funding
is provided by the District in order to achieve additional reductions
of oxides of Nitrogen (NOX). We are taking comments on this
proposal and plan to follow with a final action.

DATES: Any comments must arrive by April 11, 2016.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-R09-
OAR-2015-0819 at http://www.regulations.gov, or via email to
<EMAIL_ADDRESS>For comments submitted at Regulations.gov, follow the
online instructions for submitting comments. Once submitted, comments
cannot be edited or removed from Regulations.gov. For either manner of
submission, the EPA may publish any comment received to its public
docket. Do not submit electronically any information you consider to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Multimedia submissions (audio,
video, etc.) must be accompanied by a written comment. The written
comment is considered the official comment and should include
discussion of all points you wish to make. The EPA will generally not
consider comments or comment contents located outside of the primary
submission (i.e. on the web, cloud, or other file sharing system). For
additional submission methods, please contact the person identified in
the FOR FURTHER INFORMATION CONTACT section. For the full EPA public
comment policy, information about CBI or multimedia submissions, and
general guidance on making effective comments, please visit http://www2.epa.gov/dockets/commenting-epa-dockets.

FOR FURTHER INFORMATION CONTACT: Doris Lo, EPA Region IX, (415) 972-
3959<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION: Throughout this document, ``we,'' ``us'' and
``our'' refer to the EPA.

Table of Contents

I. Background
II. The State's Submittal
    A. What rule did the State submit?
    B. Are there other versions of the rule?
    C. What is the purpose of the submitted rule?
    D. What do the Off-Road Regulation and Rule 2449 require?
III. The EPA's Evaluation of the State's Submittal
    A. How is the EPA evaluating the rule?
    B. Does Rule 2449 meet CAA SIP evaluation criteria?
    1. Did the SCAQMD and CARB provide adequate public notice and
comment periods?
    2. Do the SCAQMD and CARB have adequate legal authority to
implement the rule?
    3. Is the rule enforceable as required under CAA section
110(a)(2)?
    4. Does the rule interfere with reasonable further progress and
attainment or any other applicable requirement of the Act?
    5. Will the State and the SCAQMD have adequate personnel and
funding for the rule?
    6. Does the rule meet the RACM and BACM requirements under CAA
sections 172(c)(1) and 189?
    7. The EPA's Rule Evaluation Conclusion
IV. Proposed Action and Public Comment
V. Incorporation by Reference
VI. Statutory and Executive Order Reviews

I. Background

    The California Air Resources Board's (CARB) Off-Road Diesel-Fueled
Fleets Regulation (13 CCR sections 2449, 2449.1 and 2449.2) applies to
fleets with nonroad \1\ compression-ignition vehicles and equipment
greater than 25 horsepower (hp). Sections 2449 and 2449.1 (collectively
the ``Off-Road

Regulation'') require fleet operators to meet a progressively more
stringent combined particulate matter (PM) and NOX standard,
or to reduce emissions through technology upgrades such as retrofit or
replacement. The Off-Road Regulation was initially approved by CARB on
July 26, 2007 and was subsequently amended in December 2010.
---------------------------------------------------------------------------

    \1\ The Clean Air Act refers to these engines as ``nonroad''
engines and the State of California uses the term ``off-road''
engines. The terms ``nonroad'' and ``off-road'' are used
interchangeably in this rule.
---------------------------------------------------------------------------

    In conjunction with the Off-Road Regulation, CARB also adopted an
``opt-in'' provision that allows local air districts to achieve
additional reductions of NOX emissions by introducing
cleaner engines or control devices into a fleet with incentive funding
(see 13 CCR section 2449.2, Surplus Off-Road Opt-In for NOX
Program (also referred to as the ``CARB SOON Program'' in today's
proposed rule)). Under this provision, any California air district can
``opt-in'' to the CARB SOON Program to achieve reductions of
NOX emissions from in-use nonroad diesel-fueled vehicles
that are surplus to what is required by CARB's Off-Road Regulation. In
order to participate in the CARB SOON Program, a district's governing
board must hold a public hearing, vote to ``opt-in'' to the CARB SOON
Program, and decide whether to make the program voluntary or mandatory.
    On May 2, 2008 the SCAQMD governing board held a public hearing at
which it voted to ``opt-in'' to the CARB SOON Program as a mandatory
requirement and adopted Rule 2449, Control of Oxides of Nitrogen
Emissions from Off-Road Diesel Vehicles, which includes by reference
the CARB SOON Program. The SCAQMD also adopted additional Rule 2449
Administrative Guidelines (May 2008) as required by the CARB SOON
Program to implement the program in the South Coast area. On July 11,
2014, the SCAQMD amended Rule 2449 to update the rule's reference to
the CARB SOON Program, which was amended by CARB in December 2011. The
SCAQMD Rule 2449 adopts the provisions of the CARB SOON Program found
under 13 CCR, section 2449.2 into the SCAQMD's rule book and makes the
CARB SOON Program a mandatory requirement for in-use off-road sources
located in the South Coast area.\2\
---------------------------------------------------------------------------

    \2\ Unless otherwise indicated, references in this notice to
Rule 2449 include the CARB Soon Program, as implemented through Rule
2449.
---------------------------------------------------------------------------

    CARB's Off-Road Regulation and the CARB SOON Program are subject to
section 209(e) of the Clean Air Act (CAA or the Act), which generally
preempts States from adopting and enforcing standards and other
requirements relating to the control of emissions from nonroad engines
(see CAA section 209(e)(1) and Engine Mfrs. Ass'n v. EPA, 88 F.3d 1075
(D.C. Cir. 1996)). However, CAA section 209(e)(2)(A) requires the EPA
to authorize California to adopt and enforce standards and other
requirements relating to the control of emissions from certain nonroad
vehicles or engines, unless the EPA makes one of three enumerated
findings. On September 20, 2013 the EPA authorized CARB to enforce the
Off-Road Regulation and the CARB SOON Program (collectively ``Fleet
Requirements'') (see 78 FR 58090-58121, September 20, 2013).
    On November 12, 2015, the EPA proposed to approve the Fleet
Requirements into the California SIP (see 80 FR 69915).\3\
---------------------------------------------------------------------------

    \3\ In particular, the EPA proposed to approve 13 CCR sections
2449 (excluding subsection 2449(d)(2)), 2449.1, and 2449.2 into the
SIP. 80 FR 69918, Table 1.
---------------------------------------------------------------------------

II. The State's Submittal

A. What rule did the State submit?

    On July 18, 2008, the State of California submitted SCAQMD Rule
2449, ``Control of Oxides of Nitrogen Emissions from Off-Road
Vehicles,'' which was adopted by the District on May 2, 2008 (see July
18, 2008 letter from Michael H. Scheible, Deputy Executive Officer,
CARB, to Wayne Nastri, Regional Administrator, EPA Region 9, with
attachments).
    On September 5, 2014, the state submitted a revision to Rule 2449
adopted by the District on July 11, 2014. The submittal made a minor
administrative revision to the numbering of the referenced CARB SOON
Program, which was revised by CARB in December 2011, from section
2449.3 to section 2449.2 (see September 5, 2014 letter to Jared
Blumenfeld, Regional Administrator, EPA Region 9, from Richard W.
Corey, Executive Officer, Air Resources Board with attachments).
    The July 18, 2008 submittal was deemed complete by operation of law
under CAA section 110(k)(1)(B) on January 18, 2009. The September 5,
2014 submittal was deemed complete by operation of law under CAA
section 110(k)(1)(B) on March 5, 2015.

B. Are there other versions of the rule?

    There are no previous versions of Rule 2449 in the SIP for the
SCAQMD.

C. What is the purpose of the submitted rule?

    NOX helps produce ground-level ozone, smog and fine
particulate matter (PM2.5), which harm human health and the
environment. Section 110(a) of the CAA requires States to submit
regulations that control NOX emissions. In addition, section
172(c)(1) of the Act requires implementation of all reasonably
available control measures (RACM) as expeditiously as practicable in
nonattainment areas. Because the South Coast area is designated
nonattainment for the 1-hour ozone standard, the 1997 annual and 24-
hour PM2.5 standard, the 2006 24-hour PM2.5
standard, the 2012 annual PM2.5 standard, the 1997 8-hour
ozone standard and the 2008 8-hour ozone standard (see 40 CFR part
81.305), CARB and the SCAQMD must implement RACM for NOX
(among other pollutants) under CAA section 172(c)(1). In addition,
under subpart 4 of the CAA, serious PM2.5 areas are required
to adopt best available control measures (BACM) for PM2.5
and its precursors.\4\ On January 13, 2016, the EPA reclassified the
South Coast PM2.5 nonattainment area as a Serious
nonattainment area for the 2006 PM2.5 NAAQS (81 FR 1514).
---------------------------------------------------------------------------

    \4\ The EPA generally takes action on a RACM or BACM
demonstration as part of our action on the State's attainment
demonstration for the relevant NAAQS.
---------------------------------------------------------------------------

    Off-road diesel vehicles collectively represent one of the largest
sources of NOX emissions in the South Coast Air Basin.\5\
The purpose of Rule 2449 is to achieve surplus NOX
reductions from this source category beyond those required under CARB's
Off-Road Regulation with funding provided by the SCAQMD. The SCAQMD's
2012 Air Quality Management Plan (AQMP) relies on NOX
reductions from Rule 2449 to attain the one-hour and 1997 eight-hour
ozone NAAQS.\6\ Rule 2449 is expected to achieve 7.5 tons per day (tpd)
of NOX reductions in 2023.\7\
---------------------------------------------------------------------------

    \5\ See, e.g., Draft Staff Report, Proposed Amended Rule 2449--
Control of Oxides of Nitrogen Emissions from Off-Road Diesel
Vehicles, page 1 (May 2014).
    \6\ See 2012 AQMP, Table 4-6, page 4-33, OFFRD-01, Extension of
the SOON Provision for Construction/Industrial Equipment
[NOX] and Appendix IV-B, pages IV-B-30 thru IV-B-32.
    \7\ Id. The EPA is not proposing to approve the emission
reductions in today's proposed rule. Emission reductions or SIP
credit from Rule 2449 will be addressed in future EPA actions on
attainment plans.
---------------------------------------------------------------------------

D. What do the Off-Road Regulation and Rule 2449 require?

    In general, CARB's Off-Road Regulation applies to all diesel-fueled
off-road fleet equipment owners operating in the State of California.
The Off-Road Regulation has performance requirements depending on the
size of the fleet (i.e., a large fleet is defined as a fleet having
greater than 5,000 horsepower (hp), a small fleet has less

than or equal to 2,500 hp, and a medium fleet is in between) \8\ and
provides calculation methodologies for determining a fleet average
index and a fleet average target rate. Each year, each subject fleet
must demonstrate that its fleet average index was less than or equal to
the applicable fleet average target rate or that it met Best Available
Control Technology (BACT) requirements by performing turnover or
installing verified diesel emission control strategies (VDECS).\9\ As
discussed above, the EPA has authorized CARB to implement the Off-Road
Regulation under CAA section 209(e) (78 FR 58090) and has proposed to
approve the Off-Road Regulation into the California SIP (80 FR 69915).
---------------------------------------------------------------------------

    \8\ See CARB's Off-Road Regulation, section 2449(c)(24),
definition of ``Fleet size category.''
    \9\ See CARB's Off-Road Regulation, section 2449.1(a) Fleet
Average Requirements, 2449.1(b) BACT Requirements, and Appendix A
with table of ``Emission Factors by Horsepower and Year (g/bhp-
hr).''
---------------------------------------------------------------------------

    SCAQMD Rule 2449 focuses on the largest fleets with the oldest
engines and requires these fleets to meet more stringent fleet average
targets than those required by section 2449.1(a) of the Off-Road
Regulation. In general, Rule 2449 applies to the owners \10\ of off-
road vehicles that operate within the SCAQMD and that are part of
fleets with more than 40 percent Tier 0 and Tier 1 vehicles \11\ (as of
January 1, 2008) and with more than 20,000 horsepower (hp) in maximum
power on a statewide basis (excluding the hp from engines in two-engine
vehicles and the hp from single cranes formerly subject to the Cargo
Handling Equipment Regulation).\12\
---------------------------------------------------------------------------

    \10\ Most provisions of the CARB SOON Program apply to fleets
rather than fleet owners or operators (see e.g. sections
2449.2(b)(2) and (d)(1)). However, SCAQMD Rule 2449 makes these
requirements applicable to the owners of off-road vehicles that
operate in SCAQMD and meet the criteria in 13 CCR 2449.2(b)(2).
    \11\ See 13 CCR section 2449(c)(48) and (49) for definitions of
Tier 0 and Tier 1 engines.
    \12\ See 13 CCR section 2449.2(b)(2), adopted by reference under
SCAQMD Rule 2449.
---------------------------------------------------------------------------

    Once the District issues a solicitation for applications for
funding under Rule 2449, subject fleet owners are required to meet the
more stringent fleet average targets required by the CARB SOON Program
or apply for incentive funding for a sufficient number of projects
(e.g., repowers, purchases, replacements) to meet the CARB SOON Program
fleet average targets (reproduced in Table 1 below).\13\
---------------------------------------------------------------------------

    \13\ See 13 CCR section 2449.2(d). Thus, for example, the Off-
Road Regulation requires ``large'' fleets to meet a fleet average
target of 1.5 g/bhp-hr for 175-750 hp engines and 3.4 g/bhp-hr for
greater than 750 hp engines in the year 2023, whereas Rule 2449 and
the CARB SOON Program require a fleet average target of 0.7 g/bhp-hr
for 175-750 hp engines and 2.7 g/bhp-hr for greater than 750 hp
engines in 2023.

                            Table 1--SOON Target for Each Max Hp Group for Use in Calculating SOON Fleet Average Target Rates
                                                                       [g/bhp-hr]
--------------------------------------------------------------------------------------------------------------------------------------------------------
         Compliance date: Jan 1 of year             25-49 hp     50-74 hp     75-99 hp    100-174 hp   175-299 hp   300-599 hp   600-750 hp    >750 hp
--------------------------------------------------------------------------------------------------------------------------------------------------------
2011............................................          5.6          6.2          6.7          6.0          5.4          5.1          5.3          6.4
2014............................................          5.8          6.5          7.1          6.4          3.9          3.7          3.7          5.3
2017............................................          5.0          5.4          5.5          4.9          2.2          2.2          2.2          4.3
2020............................................          4.1          4.2          3.4          3.1          1.4          1.3          1.4          3.4
2023............................................          3.3          3.0          1.4          1.3          0.7          0.7          0.7          2.7
--------------------------------------------------------------------------------------------------------------------------------------------------------
Source: Reproduction of Table 5 of section 2449.2(d) of CARB SOON Program. These fleet average target rates are more stringent than what is required
  under the Off-Road Regulation (see 13 CCR section 2449.1(a)(1), Table 3).

    Specifically, subject fleet owners are required to submit a report
with information on, including but not limited to, the fleet owner,
vehicle types and uses of each vehicle, engines used to power the
vehicles and the type and use of each engine, and VDECS installed on
engines. 13 CCR section 2449.2(d)(1)(A)). Fleets must calculate their
fleet average index based on the equipment they have and compare it to
the fleet average target rate based on the SOON target rates shown in
Table 1 above (13 CCR section 2449.2(d)(1)(B) and (C)), and if their
fleet average index is greater than the SOON fleet average target rate,
they are required to apply for funding (13 CCR section
2449.2(d)(1)(D)). Fleets must apply for funding in accordance with the
Carl Moyer Memorial Air Quality Standards Attainment Program (Carl
Moyer Program) \14\ policies and procedures and also with the
Administrative Guidelines \15\ adopted by the SCAQMD, which provide
further clarification on what to include in the funding applications
and compliance plans. Funding applications and compliance plans must
together demonstrate that equipment identified for the CARB SOON
Program funding will result in surplus \16\ reductions in order to
qualify for incentive funding. Once a fleet receives funding for a
qualified project, the fleet is required to implement the project. The
SCAQMD has approved significant funding for the implementation of Rule
2449. The 2012 AQMP states that the District Governing Board has
allocated up to $30 million per year for the program and extended the
SOON Program to 2023 (see Final 2012 AQMP: Appendix IV-B, p. IV-B-31).
For ``FY 2015-2016,'' or ``Year 18'' of the Carl Moyer Memorial Air
Quality Standards Attainment Program, the SCAQMD expects that
approximately $5 million of funding will be available for the SCAQMD
SOON Program (see DRAFT Technology Committee Agenda

#1, prepared for BOARD MEETING DATE: March 4, 2016, page 3).
---------------------------------------------------------------------------

    \14\ The Carl Moyer Program funds are used to fund Rule 2449
with the requirement that all projects meet, at a minimum, the Carl
Moyer Program's latest requirements and guidelines (e.g., project
selection criteria, co-funding requirements, and reporting and
monitoring requirements). For more information on the Carl Moyer
Program, see http://www.arb.ca.gov/msprog/moyer/moyer.htm.
    \15\ In addition to the Carl Moyer Program guidelines, the CARB
SOON Program requires the District to adopt District guidelines,
through a public process, that include additional administrative
provisions necessary to implement the CARB SOON Program. These
provisions include, but are not limited to, funding guidelines,
compliance planning requirements and reporting and monitoring
requirements. The SCAQMD adopted these additional district
guidelines on May 22, 2008 (see Draft Administrative Guidelines,
Proposed Rule 2449 Administrative Guidelines, SCAQMD, May 2008). The
SCAQMD Board plans to consider amendments to the May 2008
Administrative Guidelines on March 4, 2016 (see DRAFT Technology
Committee Agenda #1, prepared for BOARD MEETING DATE: March 4, 2016,
with Attachment 4, SOON Provision Implementation Guidelines). The
amendments include referencing the correct section of CARB's Off-
Road Regulation and aligning funding levels for the SCAQMD SOON
Program with the Carl Moyer program. If approved by the SCAQMD
Board, the EPA expects the SCAQMD to forward the amendments to CARB
for approval.
    \16\ Surplus reductions are those NOX reductions that
are not needed for meeting the requirements of the Off-Road
Regulation. If surplus reductions are available and used to meet the
requirements of Rule 2449 and the CARB SOON Program, then those
reductions cannot be used to meet the requirements of the Off-Road
Regulation until they are no longer needed for compliance with Rule
2449.
---------------------------------------------------------------------------

III. The EPA's Evaluation of the State's Submittal

A. How is the EPA evaluating the rule?

    The EPA has evaluated Rule 2449 against the applicable procedural
and substantive CAA requirements for SIPs and SIP revisions and has
concluded that it meets all of the applicable requirements.
    Generally, SIPs must include enforceable emission limitations and
other control measures, means, or techniques, as well as schedules and
timetables for compliance, as may be necessary to meet the requirements
of the Act (see CAA section 110(a)(2)(A)); must provide necessary
assurances that the State will have adequate personnel, funding, and
authority under State law to carry out such SIP (and is not prohibited
by any provision of Federal to State law from carrying out such SIP)
(see CAA section 110(a)(2)(E)); must be adopted by a State after
reasonable notice and public hearing (see CAA section 110(l)), and must
not interfere with any applicable requirement concerning attainment and
reasonable further progress, or any other applicable requirement of the
Act (see CAA section 110(l)).\17\
---------------------------------------------------------------------------

    \17\ CAA section 193, which prohibits any pre-1990 SIP control
requirement relating to nonattainment pollutants in nonattainment
areas from being modified unless the SIP is revised to insure
equivalent or greater emission reductions of such air pollutants,
does not apply to this rule because it does not include any pre-1990
SIP control requirements.
---------------------------------------------------------------------------

    In addition, as noted above, CARB and the SCAQMD must implement
RACM for NOX (among other pollutants) under CAA section
172(c)(1).

B. Does Rule 2449 meet CAA SIP evaluation criteria?

1. Did the SCAQMD and CARB provide adequate public notice and comment
periods?
    Under CAA section 110(l), SIP revisions must be adopted by the
State, and the State must provide for reasonable public notice and
hearing prior to adoption. In 40 CFR 51.102(d), we specify that
reasonable public notice in this context refers to at least 30 days.
The State has submitted evidence of public notice and hearing prior to
the May 5, 2008 adoption and July 11, 2014 amendment of Rule 2449 by
the SCAQMD (see attachments to July 18, 2008 letter to Mr. Wayne
Nastri, EPA Region 9 from Michael H. Scheible, Air Resource Board and
attachments to September 5, 2014 letter to Mr. Jared Blumenfeld, EPA
Region 9, from Richard W. Corey, Air Resources Board). Based on the
evidence provided by the SCAQMD and CARB, we conclude that they have
provided adequate public notice and comment periods.
2. Do the SCAQMD and CARB have adequate legal authority to implement
the rule?
    California air districts are authorized to adopt and enforce rules
by California Health and Safety Code (H&SC) section 40001. CARB is
authorized to adopt the rules as revisions to the SIP by H&SC section
39601, 39602, and 41650 through 41652 (see CARB Executive Order S-14-
012).
    In addition, we note that California H&SC sections 43013(a) and
43018 provide CARB with broad authority to achieve the maximum feasible
and cost-effective emission reductions from all mobile source
categories, including both on-road and off-road diesel engines.
    As discussed above, CARB's Off-Road Regulation is subject to CAA
section 209(e), and on September 20, 2013 the EPA granted CARB's
request for authorization to enforce its Fleet Requirements, including
the CARB SOON Program (see 78 FR 58090-58121, September 20, 2013).
Thus, we find that the SCAQMD and CARB have adequate legal authority to
adopt and implement Rule 2449.
3. Is the rule enforceable as required under CAA section 110(a)(2)?
    We have evaluated the enforceability of Rule 2449 and the CARB SOON
Program with respect to applicability and exemptions; standard of
conduct and compliance dates; sunset provisions; discretionary
provisions; and test methods, recordkeeping and reporting,\18\ and have
concluded for the reasons given below that the rule is enforceable for
the purposes of CAA section 110(a)(2).
---------------------------------------------------------------------------

    \18\ These concepts are discussed in detail in an EPA memorandum
from J. Craig Potter, EPA Assistant Administrator for Air and
Radiation, et al., titled ``Review of State Implementation Plans and
Revisions for Enforceability and Legal Sufficiency,'' dated
September 23, 1987.
---------------------------------------------------------------------------

    First, with respect to applicability, we find Rule 2449 and the
CARB SOON Program to be sufficiently clear as to which fleet owners and
which vehicles or engines are subject to the program and the rule (see
Rule 2449 and 13 CCR section 2449.2(b)). In general, the rule applies
to owners of vehicles that operate within the SCAQMD and are part of a
fleet consisting of 40 percent Tier 0 and Tier 1 vehicles with greater
than 20,000 hp statewide, excluding the hp from engines in two-engine
vehicles and single engine cranes formerly subject to the Cargo
Handling Equipment Regulation (see 13 CCR 2449.2(b)(2)).
    Second, we find that Rule 2449 and the CARB SOON Program are
sufficiently specific so that the persons affected are fairly on notice
as to what the requirements and related compliance dates are. We have
described the substantive requirements and compliance dates set forth
in Rule 2449 in section II.D. of today's proposed rule.
    Third, the requirements of Rule 2449 will sunset at different times
from 2011 through 2023, depending on when the SCAQMD issues its
solicitations for funding; however, once a fleet is no longer subject
to Rule 2449, it will be then be subject to the requirements of the
Off-Road Regulation.
    Fourth, Rule 2449 contains a provision that allows for discretion
on the part of CARB's Executive Officer (EO), this provision is limited
both in scope and application, and is no longer relevant since the date
to request discretion has passed (see 13 CCR section 2449.2(e)(2),
allowing a fleet to apply to the EO for an extension from the
requirements if the rule calculations would require a fleet to turn
over Tier 2 or better engines before January 1, 2014). As such, we find
that this provision does not undermine the enforceability of Rule 2449
or preclude its approval into the SIP.
    Lastly, Rule 2449 identifies appropriate calculation requirements
and includes adequate recordkeeping and reporting requirements
sufficient to ensure compliance with the applicable requirements. In
particular, as described above, once the SCAQMD issues a solicitation,
each subject fleet owner must submit a report containing detailed
information about each vehicle and engine in the fleet, each VDECS
installed on an engine in the fleet, and other information related to
compliance with the Off-Road Rule (see 13 CCR 2449(d)(1)(A) and
2449(g). If the fleet average index is greater than the SOON fleet
average target rate, the fleet owner must apply for SOON funding (13
CCR 2449.2(d)(1)(B)). If the necessary NOX retrofits,
repower, or vehicle replacements are available, the application must
indicate how these retrofits, repowers, or vehicle replacements would
bring the fleet average index for vehicles that operate within the
SCAQMD to less than or equal to the SOON fleet average target rate (13
CCR 2449.2(d)(1)(D)). In addition, the fleet owner must prepare and
submit a compliance plan laying out the actions it is required to take

under section 2449.1 and the actions for which it is applying to the
SCAQMD for funding under section 2449.2 (13 CCR 2449.2(e)(3)).
4. Does the rule interfere with reasonable further progress and
attainment or any other applicable requirement of the Act?
    As discussed above, the SCAQMD's 2012 AQMP relies on NOX
reductions from Rule 2449 to attain the one-hour and 1997 eight-hour
ozone NAAQS. The EPA has approved SCAQMD's commitment to implement the
SOON Program as part of the SCAQMD's aggregate NOX emissions
reductions commitment (see 79 FR 29712, 29720 and 29721). Approval of
Rule 2449 into the SIP will help fulfill this commitment. Thus, the EPA
believes that approval of Rule 2449 does not interfere with Reasonable
Further Progress, attainment or any other applicable requirement of the
Act.
5. Will the State and the SCAQMD have adequate personnel and funding
for the rule?
    As discussed above, the SCAQMD has approved significant funding for
the implementation of Rule 2449. The 2012 AQMP states that the SCAQMD
Board has allocated up to $30 million per year for the program and
extended the SOON Program to 2023 (see Final 2012 AQMP: Appendix IV-B,
p. IV-B-31). For ``FY 2015-2016,'' or ``Year 18'' of the Carl Moyer
Memorial Air Quality Standards Attainment Program, the SCAQMD expects
to have approximately $5 million of funding available for the SCAQMD
SOON Program (see DRAFT Technology Committee Agenda #1, prepared for
BOARD MEETING DATE: March 4, 2016, page 3).
6. Does the rule meet the RACM and BACM requirements under CAA sections
172(c)(1) and 189?
    Rule 2449 provides for the most stringent in-use off-road diesel
equipment requirements that we are aware of in the United States, and
thus, we find that the rule implements both reasonably available and
best available control measures for this source category. However, as
discussed above, the EPA generally takes action on a RACM or BACM
demonstration as part of our action on the State's attainment
demonstration for the relevant NAAQS. Thus, while we do not know of any
more stringent requirements for this category at this time, we are also
not taking any action on how this measure fits within the context of a
RACM or BACM demonstration for the South Coast area.
7. The EPA's Rule Evaluation Conclusion
    Based on the above discussion, we believe Rule 2449 and the CARB
SOON Program are consistent with the relevant CAA requirements,
policies and guidance.

IV. Proposed Action and Public Comment

    As authorized in section 110(k)(3) of the Act, the EPA is proposing
to fully approve the submitted rule because we believe it fulfills all
relevant requirements. We will accept comments from the public on this
proposal until April 11, 2016. Unless we receive convincing new
information during the comment period, we intend to publish a final
approval action that will incorporate this rule into the federally
enforceable SIP.

V. Incorporation by Reference

    In this rule, the EPA is proposing to include in a final EPA rule
regulatory text that includes incorporation by reference. In accordance
with requirements of 1 CFR 51.5, the EPA is proposing to incorporate by
reference SCAQMD Rule 2449. The EPA has made, and will continue to
make, this document available electronically through
www.regulations.gov and in hard copy at the appropriate EPA office (see
the ADDRESSES section of this preamble for more information).

VI. Statutory and Executive Order Reviews

    Under the CAA, the Administrator is required to approve a SIP
submission that complies with the provisions of the Act and applicable
Federal regulations. 42 U.S.C. 7410(k); 40 CFR 52.02(a). Thus, in
reviewing SIP submissions, the EPA's role is to approve State choices,
provided that they meet the criteria of the Act. Accordingly, this
proposed action merely proposes to approve State law as meeting Federal
requirements and does not impose additional requirements beyond those
imposed by State law. For that reason, this proposed action:
     Is not a ``significant regulatory action'' subject to
review by the Office of Management and Budget under Executive Order
12866 (58 FR 51735, October 4, 1993);
     does not impose an information collection burden under the
provisions of the Paperwork Reduction Act (44 U.S.C. 3501 et seq.);
     is certified as not having a significant economic impact
on a substantial number of small entities under the Regulatory
Flexibility Act (5 U.S.C. 601 et seq.);
     does not contain any unfunded mandate or significantly or
uniquely affect small governments, as described in the Unfunded
Mandates Reform Act of 1995 (Pub. L. 104-4);
     does not have Federalism implications as specified in
Executive Order 13132 (64 FR 43255, August 10, 1999);
     is not an economically significant regulatory action based
on health or safety risks subject to Executive Order 13045 (62 FR
19885, April 23, 1997);
     is not a significant regulatory action subject to
Executive Order 13211 (66 FR 28355, May 22, 2001);
     is not subject to requirements of Section 12(d) of the
National Technology Transfer and Advancement Act of 1995 (15 U.S.C. 272
note) because application of those requirements would be inconsistent
with the CAA; and
     does not provide the EPA with the discretionary authority
to address disproportionate human health or environmental effects with
practical, appropriate, and legally permissible methods under Executive
Order 12898 (59 FR 7629, February 16, 1994).
    In addition, the SIP is not approved to apply on any Indian
reservation land or in any other area where the EPA or an Indian tribe
has demonstrated that a tribe has jurisdiction. In those areas of
Indian country, the rule does not have tribal implications and will not
impose substantial direct costs on tribal governments or preempt tribal
law as specified by Executive Order 13175 (65 FR 67249, November 9,
2000).

List of Subjects in 40 CFR Part 52

    Environmental protection, Air pollution control, Incorporation by
reference, Intergovernmental relations, Nitrogen dioxide, Ozone,
Particulate matter, Reporting and recordkeeping requirements.

    Authority:  42 U.S.C. 7401 et seq.

    Dated: February 25, 2016.
Jared Blumenfeld,
Regional Administrator, Region IX.
[FR Doc. 2016-05278 Filed 3-9-16; 8:45 am]
 BILLING CODE 6560-50-P


[Federal Register: April 26, 2011 (Volume 76, Number 80)]
[Proposed Rules]
[Page 23221-23222]
[DOCID:fr26ap11-17]

=======================================================================
-----------------------------------------------------------------------

COMMODITY FUTURES TRADING COMMISSION

17 CFR Chapter I

SECURITIES AND EXCHANGE COMMISSION

17 CFR Chapter II

[Release No. 34-64314; File No. 4-625]

Joint Public Roundtable on Issues Related to the Schedule for
Implementing Final Rules for Swaps and Security-Based Swaps Under the
Dodd-Frank Wall Street Reform and Consumer Protection Act

AGENCIES: Commodity Futures Trading Commission (``CFTC'') and
Securities and Exchange Commission (``SEC'') (each, an ``Agency,'' and
collectively, the ``Agencies'').

ACTION: Notice of roundtable discussion; request for comment.

-----------------------------------------------------------------------

SUMMARY: On Monday, May 2, 2011, and Tuesday, May 3, 2011, commencing
each day at 9:30 a.m. and ending at 4 p.m., staff of the Agencies will
hold a public roundtable meeting at which invited participants will
discuss various issues related to the schedule for implementing final
rules for swaps and security-based swaps under the Dodd-Frank Wall
Street Reform and Consumer Protection Act (the ``Act''). The discussion
will be open to the public with seating on a first-come, first-served
basis. Members of the public may also listen to the meeting by
telephone. Call-in participants should be prepared to provide their
first name, last name and affiliation. The information for the
conference call is set forth below.
     U.S. Toll-Free:<PHONE_NUMBER>.
     International Toll: information on international dialing
can be found at the following link: http://www.cftc.gov/PressRoom/
PressReleases/internationalnumbers021811.html.
     Conference ID: 1212444.
    A transcript of the public roundtable discussion will be published
at http://www.cftc.gov/PressRoom/Events/2011/index.htm. The roundtable
discussion will take place each day in the Conference Center at the
CFTC's headquarters, Three Lafayette Centre, 1155 21st Street, NW.,
Washington, DC.

FOR FURTHER INFORMATION CONTACT: The CFTC's Office of Public Affairs at
(202) 418-5080 or the SEC's Office of Public Affairs at<PHONE_NUMBER>.

SUPPLEMENTARY INFORMATION: The roundtable discussion will take place on
Monday, May 2, 2011, and Tuesday, May 3, 2011, commencing each day at
9:30 a.m. and ending at 4 p.m. Members of the public who wish to
comment on the topics addressed at the discussion, or on any other
topics related to the schedule for implementing final rules for swaps
and security-based swaps under the Act, may do so via:
     Paper submission to David Stawick, Secretary, Commodity
Futures Trading Commission, Three Lafayette Centre, 1155 21st Street,
NW., Washington, DC 20581, or Elizabeth M. Murphy, Secretary,
Securities and Exchange Commission, 100 F Street, NE., Washington, DC
20549-1090; or
     Electronic submission via visiting http://
comments.cftc.gov/PublicComments/CommentForm.aspx?id=1000 and
submitting comments through the CFTC's Web site; and/or by e-mail to
<EMAIL_ADDRESS>(all e-mails must reference the file number 4-625
in the subject field) or through the comment form available at: http://
www.sec.gov/rules/other.shtml.
    All submissions will be reviewed jointly by the Agencies. All
comments must be in English or be accompanied by an English
translation. All submissions provided to either Agency in any
electronic form or on paper will be published on the Web site of the
respective Agency, without review and without removal of personally
identifying information. Please submit only information that you wish
to make publicly available.

    By the Commodity Futures Trading Commission.

    Dated: April 20, 2011.
David A. Stawick,
Secretary.

    By the Securities and Exchange Commission.

    Dated: April 20, 2011.
Elizabeth M. Murphy,
Secretary.

Concurring Statement of CFTC Commissioner Scott D. O'Malia;
Implementation Roundtable Seriatim; Certainty & Transparency

    I concur in supporting the Commission's roundtable on the
implementation process.

    Along with the Chairman, I believe that our entire rulemaking
process should be as transparent as possible to the public.
Consequently, after the Roundtable is complete, I strongly recommend
that the Commission submit both a proposal on the order in which the
Commission will consider final rulemakings and a proposed
implementation plan to the Federal Register to allow the public to
comment before we begin to consider final rules. Once we receive and
review comments, a final rulemaking and implementation schedule should
be published in the Federal Register. This level of transparency will
give the market a clear picture of how the Commission intends to
proceed, and how we can be held accountable as we undertake this
massive regulatory overhaul. It will also provide the market with
certainty market participants need to make the critical investment
decisions necessary to be in compliance with the rules upon
implementation. Finally, this type of transparency will help guide the
Commission's decision regarding when to make critical investments in
advanced technology that are necessary for us to effectively oversee
the futures, options, and swaps markets.
    The more thoughtful, deliberate, and transparent our sequencing and
implementation processes are, the more orderly this Commission's
regulation of the swaps market will be.

[FR Doc. 2011-10158 Filed 4-25-11; 8:45 am]
BILLING CODE 8011-01-P; 6351-01-P


[Federal Register: May 24, 2006 (Volume 71, Number 100)]
[Notices]
[Page 29929]
[DOCID:fr24my06-53]

-----------------------------------------------------------------------

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. CP06-168-000]

CenterPoint Energy Gas Transmission Company; Notice of Request
under Blanket Authorization

May 16, 2006.
    Take notice that on May 1, 2006, CenterPoint Energy Gas
Transmission Company (CEGT), 1111 Louisiana Street, Houston, Texas
77002-5231, filed in Docket No. CP06-168-000 a request pursuant to
sections 157.205 and 157.208(b) of the Commission's Regulations under
the Natural Gas Act (18 CFR 157.205 and 157.208) for authorization to;
abandon in place, replace and extend an existing supply lateral;
construct a new compressor station; and increase the maximum allowable
operating pressure (MAOP) of the line, located in Bienville and Webster
Parishes, Louisiana, under the authorization issued in Docket Nos.
CP82-384-000 and CP82-384-001 pursuant to Section 7 of the Natural Gas
Act, all as more fully described in the request.
    This filing is available for review at the Commission in the Public
Reference Room or may be viewed on the Commission's Web site at http://www.ferc.gov
 using the ``eLibrary'' link. Enter the docket number

excluding the last three digits in the docket number field to access
the document. For assistance, please contact FERC Online Support at
<EMAIL_ADDRESS>or toll-free at<PHONE_NUMBER>, or for TTY,

contact<PHONE_NUMBER>.
    Any questions concerning this request may be directed to Lawrence
O. Thomas, Director of Rates and Regulatory, CenterPoint Energy Gas
Transmission Company, P.O. Box 21734, Shreveport, Louisiana 71151, at
(318) 429-2804.
    CEGT proposes to construct approximately 17.5 miles of 12-inch
pipeline to replace and extend Line FT-2 and to increase its MAOP from
450 psig to 1000 psig. CEGT indicates that the replacement and
extension would require new and additional right-of-way. CEGT also
proposes to abandon in place the existing 14-inch mechanically-coupled
pipe.
    CEGT, in addition, proposes to construct the Sibley Compressor
Station that would consist of two (2) 1550 hp Waukesha L7044GSI
compressor units and appurtenant facilities. CEGT states that all of
the proposed construction activities would occur in Bienville and
Webster Parishes, Louisiana.
    CEGT contends that the proposed construction, abandonment, and
increase in MAOP would have no adverse affect on any existing customers
or service. It is said that the total estimated construction cost would
be approximately $18.1 million, which would be financed with available
funds and/or short-term borrowings.
    Any person or the Commission's Staff may, within 45 days after the
issuance of the instant notice by the Commission, file pursuant to Rule
214 of the Commission's Procedural Rules (18 CFR 385.214) a motion to
intervene or notice of intervention and, pursuant to section 157.205 of
the Commission's Regulations under the Natural Gas Act (NGA) (18 CFR
157.205) a protest to the request. If no protest is filed within the
time allowed therefore, the proposed activity shall be deemed to be
authorized effective the day after the time allowed for protest. If a
protest is filed and not withdrawn within 30 days after the time
allowed for filing a protest, the instant request shall be treated as
an application for authorization pursuant to section 7 of the NGA.
    Comments, protests and interventions may be filed electronically
via the Internet in lieu of paper. See, 18 CFR 385.2001(a)(1)(iii) and
the instructions on the Commission's Web site under the ``e-filing''
link. The Commission strongly encourages electronic filings.

Magalie R. Salas,
Secretary.
[FR Doc. E6-7881 Filed 5-23-06; 8:45 am]

BILLING CODE 6717-01-P