An Evaluation of the Human Carcinogenic Potential of Ethylene Glycol Butyl Ether National Center for Environmental Assessment Office of Research and Development U. S. Environmental Protection Agency August 2003 ( INTERIM FINAL)

NOTICE This document is intended for internal use only and presents the Agency's interim position based on the available information. It has not been formally released by the U. S. Environmental Protection Agency and should not at this stage be construed to represent the Agency's final position on this chemical.

U. S. Environmental Protection Agency Washington D. C. AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE ii DISCLAIMER This document is intended for internal use only and presents the Agency's interim position based on the available information. It has not been formally released by the U. S. Environmental Protection Agency and should not at this stage be construed to represent the Agency's final position on this chemical. Mention of trade names or commercial products does not constitute endorsement or recommendation for use. AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE iii TABLE OF CONTENTS AUTHORS, CONTRIBUTORS, AND REVIEWERS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv EXECUTIVE SUMMARY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 ATTACHMENT 1: Forestomach Tumors in Female Mice . . . . . . . . . . . . . . . . . . . . . . . . . . A1 1 ATTACHMENT 2: Liver Hemangiosarcoma and Hepatocellular Carcinoma in Male Mice . A2 1 ATTACHMENT 3: Benchmark Dose Assessment of Forestomach Lesions in Female Mice Using PBPK Models to Estimate Human Equivalent Exposures . . A3 1 ATTACHMENT 4: External Peer Review   Summary of Comments and Disposition . . . . . A4 1 AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE iv AUTHORS AND REVIEWERS Primary Author Jeff Gift, Ph. D. U. S. EPA National Center for Environmental Assessment Internal EPA Reviewers Jennifer Jinot, Ph. D. U. S. EPA National Center for Environmental Assessment Jean Parker, Ph. D. U. S. EPA Office of Prevention, Pesticides and Toxic Substances Paul White, Ph. D. U. S. EPA National Center for Environmental Assessment John Lipscomb, Ph. D. U. S. EPA National Center for Environmental Assessment Larry Valcovich, Ph. D. U. S. EPA National Center for Environmental Assessment Michel Stevens, Ph. D. U. S. EPA National Center for Environmental Assessment External Peer Reviewers Burhan I. Ghanayem, Ph. D. National Institute of Environmental Health Sciences Dale Hattis, Ph. D. Center for Technology, Environment, and Development ( CENTED)

Philip Leber, Ph. D. The Goodyear Tire & Rubber Co.

Andrew Gale Salmon M. A., D. Phil., C. Chem., M. R. S. C. California EPA Office of Environmental Health Hazard Assessment AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE v Michael D. Shelby, Ph. D. Director, NTP Center for the Evaluation of Risks to Human Reproduction Summaries of the external peer reviewers' comments and the disposition of their recommendations are in Attachment 4. AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 1 An Evaluation of the Human Carcinogenic Potential of Ethylene Glycol Butyl Ether EXECUTIVE SUMMARY Since the publication of NTP's draft report ( NTP, 1998) on their 2 year inhalation bioassay of ethylene glycol butyl ether ( EGBE; 2 butoxyethanol), there has been continued discussion among scientists from government, industry, and academia concerning the human carcinogenic potential of EGBE. NTP ( 1998; 2000) reported that their study results indicate no evidence of carcinogenic activity in male F344/ N rats, equivocal evidence of carcinogenic activity in female F344/ N rats based on increased combined incidence of benign and malignant pheochromocytomas,

some evidence of carcinogenic activity in male B6C3F1 mice based on increased incidence of hemangiosarcomas of the liver, and some evidence of carcinogenic activity in female B6C3F1 mice based on increased incidence of forestomach squamous cell papillomas or carcinomas. The U. S.

Environmental Protection Agency ( EPA) IRIS ( Integrated Risk Information System) assessment ( U. S. EPA, 1999a) concluded that, in accordance with the proposed Guidelines for Carcinogen Risk Assessment ( U. S. EPA, 1996), the human carcinogenicity of EGBE " cannot be determined at this time, but suggestive evidence exists from rodent studies." Under the pre existing EPA guidelines ( U. S. EPA, 1986), EGBE was judged to be a possible human carcinogen." These findings by EPA and NTP prompted investigators, largely supported by the Glycol Ethers Panel of the American Chemistry Council, to design research projects aimed at determining the mode of action for the formation of the forestomach and liver tumors observed in mice. In this paper,

recent findings reported in scientific publications and meetings and EPA interim ( U. S. EPA, 1The increased incidence of pheochromocytomas reported by NTP is not addressed here because these tumors were reported to have been difficult to distinguish, were not statistically increased over chamber controls, and were not a contributing factor in the IRIS assessment of human carcinogenic risk from EGBE exposure ( U. S. EPA, 1999a).

AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 2 1999b) and draft final ( U. S. EPA, 2003) cancer guidelines are used to provide an up to date evaluation of the mode of action involved in the origin of these tumors1 in mice and their human relevance.

Establishing the mode of action is critical for determining relevance to humans and for choosing the approach most appropriate for dose response modeling ( i. e., whether to use a linear or nonlinear approach). As is extensively discussed in the Agency's interim and draft cancer guidelines ( U. S. EPA, 1999b; 2003), in order to determine a chemical's mode of action, one must consider the full range of key influences a chemical or its metabolites might have as an initiator or promoter of the complex carcinogenic process. With this in mind, EGBE's role in the formation of female mouse forestomach ( Attachment 1) and male mouse liver ( Attachment 2) tumors observed following two years of inhalation exposure ( National Toxicology Program, 2000) were evaluated.

These assessments are summarized below.

Forestomach papillomas and carcinoma in female mice Table 1 summarizes the dose response data for key tumor types observed in female mice in the NTP ( 2000) inhalation study of EGBE. At the 250 ppm exposure level, the 10% incidence of squamous cell papillomas and 12% combined incidence of squamous cell papillomas or carcinomas AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 3 were significantly increased over study controls and exceeded the ranges for historical controls of 0 2% and 0 3%, respectively. NTP ( 2000) reports that 8% is the highest incidence of forestomach neoplasms that has been observed in contemporary historical controls. NTP ( 2000) did not observe significant increases in forestomach papillomas and carcinomas at other exposure levels in female mice, nor at any exposure level in male mice or either sex of rats.

Recent reviews of available in vitro and in vivo genotoxicity assays are in agreement that EGBE is not likely to be genotoxic ( Commonwealth of Australia, 1996; Elliot and Ashby, 1997;

U. S. EPA, 1999a; NTP, 2000). NTP ( 2000) suggested that EGBE caused chronic irritation leading to forestomach injury including penetrating ulcers and that the observed " neoplasia [ papillomas and one carcinoma] was associated with a continuation of the injury/ degeneration process." Table 2 provides a summary of the strength of the evidence and the relevance to humans of this nongenotoxic and nonlinear mode of action for EGBE's role in the formation of these forestomach papillomas and carcinomas ( Cantox, 2000; NTP, 2000; Green et al., 2002; Poet et.

al., 2003).

The Agency believes that a nonlinear mode of action similar to that which is represented in Table 2 and described further in Attachment 1, is principally responsible for the increased forestomach tumor incidence reported by NTP ( 2000). However, reports of weak positive effects by EGBE at high concentrations in some in vitro DNA repair, sister chromatic exchange and cell transformation assays ( see discussion in Attachment 1 under " Other Possible Modes of Action for AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 4 Forestomach Tumor Development in Female Mice") make it difficult to completely exclude the potential for contribution from direct interaction of an EGBE metabolite with DNA. While these positive findings may be due to study design artifacts ( e. g., changes in pH or osmolarity associated with high EGBE concentrations), they may also be due to butoxyacetaldehyde ( BAL), a shortlived metabolite of EGBE that has caused clastogenic changes in Chinese hamster lung ( V79) and human lymphocyte cells ( Elliot and Ashby, 1997). As is discussed in Attachment 1, available evidence from a published EGBE PBPK model that has been modified to include kinetics for the metabolism of the BAL intermediate ( Corley, 2003) suggests that the conditions of these in vitro assays ( e. g., no metabolic activation; high, cytotoxic concentrations of BAL) are of little relevance to expected target organ ( forestomach) environment ( e. g., high metabolic activity; low concentrations of BAL). However, additional research ( e. g., verification of these PBPK modeling results and further genotoxicity research using more appropriate assays and currently accepted test protocols) is needed before a more definitive determination can be made regarding the role of BAL in the formation of forestomach tumors in female mice.

Liver Tumors in Male Mice Table 3 summarizes the data for tumor types which were significantly increased in male mice exposed to EGBE by NTP ( 2000). Particular focus has been placed on hemangiosarcomas of the liver because this was the only tumor type that was increased over both concurrent and historical controls and because a mode of action involving EGBE has been proposed for this tumor AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 5 ( Siesky et al., 2002). Though the incidence of hepatocellular carcinomas was within the range of historical controls for male mice, consideration was given to this tumor because the dose response trend is significant and because a similar mode of action has been suggested for this tumor.

Table 4 summarizes the strength of the evidence and the relevance to humans of the mode of action described in Attachment 2 for EGBE's potential role in the formation of hemangiosarcomas and hepatocellular carcinomas in the livers of male mice. A metabolite of EGBE, butoxyacetic acid ( BAA), has long been known to cause hemolysis in rodents ( Carpenter et al, 1956). This hemolysis leads to the accumulation of hemosiderin ( iron) in phagocytic Kupffer cells of the liver of both rats and mice ( NTP, 2000). Recent research in mice and rats indicates that the increased iron levels associated with EGBE induced hemolysis produces liver oxidative damage that is more severe in mice and increased DNA synthesis in both endothelial cells and hepatocytes that is unique to mice ( Siesky et al., 2002). It is hypothesized that these events can contribute to the transformation of the endothelial cells to hemangiosarcomas and hepatocytes to hepatocellular carcinomas in male mice. Given the high background rate of these two tumor types in male mice ( 2.9% and 24%) relative to female mice ( 0.9% and 14%) and rats ( 0% and 0.4%;

combined male and female) ( NTP, 2002), it is reasonable to hypothesize that the endothelial cells and hepatocytes in the livers of male mice are more susceptible to oxidative stress resulting from iron buildup in local Kupffer cells. While additional research would be informative with respect to mechanistic issues such as the relative susceptibility of endothelial cells and hepatocytes to oxidative stress caused by the hemolytic effects of EGBE and the apparent resistance of female AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 6 mice to the development of hemangiosarcomas despite experiencing similar hemolytic effects, there is enough evidence at this time to support an EPA determination that events associated with hemolysis contributed to the increased incidence of these tumors in male mice exposed to EGBE.

Available evidence appears to support a nonlinear mode of action similar to the one described here and in Attachment 2 as principally responsible for the increased liver tumor incidence reported by NTP ( 2000) for male mice. However, as described above for forestomach tumors observed in female mice, the weak positive effects by EGBE in some in vitro genotoxicity assays and the reported clastogenicity of the EGBE metabolite ( BAL) make it difficult to completely exclude the potential for contribution from direct interaction of an EGBE metabolite with DNA. As is discussed in Attachment 2, the Corley ( 2003) PBPK model suggests that the conditions of these in vitro assays ( e. g., no metabolic activation; high, cytotoxic concentrations of BAL) are of little relevance to expected target organ ( liver) environment ( e. g., high metabolic activity; low concentrations of BAL). Here again, additional research ( e. g., verification of the PBPK modeling results and improved genotoxicity research) is needed before a more definitive determination can be made regarding the role of BAL in the formation of liver tumors in male mice. 2These analyses are consistent with the nonlinear assessment approach described in existing interim ( U. S. EPA, 1999a) and draft ( 2003) cancer guidelines.

AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 7 Risk to Humans Forestomach tumors in female mice  Available data establish a plausible nonlinear,

nongenotoxic mode of action for the moderate increase observed by NTP ( 2000) in the incidence of forestomach tumors in female mice following chronic inhalation exposure to EGBE.

Forestomach tissue irritation caused by constant exposure to EGBE and its metabolites and subsequent cell proliferation appear to be key precursor events in the mode of action for these tumors. While certain dosimetric processes and morphological aspects of the forestomach make rodents particularly susceptible to these events, this mode of action is judged to be of qualitative relevance to humans. However, due to the lack of a comparable organ for storage and the long term retention of EGBE, the exposure concentrations that would be necessary to cause hyperplastic effects and tumors in humans, if attainable, are likely to be much higher than the concentrations necessary to cause forestomach effects in mice. In fact, the analysis in Attachment 3 indicates that the exposure concentrations necessary to cause hyperplastic effects in humans would be much higher than the existing RfD and RfC for EGBE. Given that humans, including potentially sensitive subpopulations such as children, have no known organ for the retention of a comparable target dose of EGBE or its metablolites, it appears reasonable to assume that the RfC and RfD developed for EGBE ( EPA, 1999a) are sufficient for the prevention of hyperplasia and associate tumors in humans. 2 3These analyses are consistent with the nonlinear assessment approach described in existing interim ( U. S. EPA, 1999a) and draft ( 2003) cancer guidelines.

AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 8 Liver tumors in male mice  Available data establish a plausible nonlinear, nongenotoxic mode of action for the moderate increase observed by NTP ( 2000) in the incidence of liver tumors in male mice following chronic inhalation exposure to EGBE. The proposed mode of action suggests that the endothelial cells and hepatocytes of male mice are sensitive to the formation of the subject neoplasms ( as evidenced by the relatively high background rate of these tumors in male mice) and that excess iron from EGBE induced hemolysis can result in sufficient iron induced oxidative stress to cause the observed, marginal increase in the incidence of liver hemangiosarcomas and hepatocellular carcinomas in these animals ( NTP, 2000). Given the relatively low sensitivity of humans, including subpopulations such as children, to the hemolytic effects of EGBE, it appears reasonable to assume that the EGBE RfC and RfD ( EPA, 1999a) are sufficient for the prevention of hemolysis and associate tumors in humans. 3 Conclusion Concerning EGBE's Cancer Risk  Information available to the Agency at this time indicate that nonlinear modes of action are likely responsible for the increased incidence of tumors observed by NTP ( 2000) in mice following chronic EGBE exposure. Application of nonlinear quantitative assessment methods indicate that the noncancer RfD ( 0.5 mg/ kg/ day) and RfC ( 13 mg/ m3) values developed for EGBE ( EPA, 1999a) are adequately protective of these carcinogenic effects. However, this determination assumes a nonlinear mechanism that requires exposure levels to be high enough to cause certain lesions that are considered to be precancerous.

Information is currently inadequate to dismiss the potential contribution of a linear mechanism AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 9 associated with the possible mutagenic metabolite BAL. A definitive determination regarding the appropriateness of a nonlinear approach can not be made until questions regarding the role of BAL are resolved. As discussed above, additional research ( e. g., verification of existing PBPK modeling results and improved genotoxicity assays) would assist the Agency in making a more informed decision concerning the potential for BAL to contribute to the adverse effects seen in animals following EGBE exposure and use of the proposed nonlinear assessment approach. 4Poly 3 test estimate taken from NTP, 2000 technical report series 484 AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 10 Table 1  Key Tumors Observed in Female Mice Exposed to EGBE ( NTP, 2000)

Control 62.5 ppm 125 ppm 250 ppm Squamous Cell Papilloma  Forestomach Overall rate Rate adjusted for intercurrent mortality4 First incidence ( days) 0/ 50 0% 0% NA 1/ 50 2% 2.4% 731 2/ 50 4% 4.8% 731 5/ 50 10% 11.2% 582 Squamous Cell Papilloma or Carcinoma  Forestomach Overall rate Rate adjusted for intercurrent mortality First incidence ( days) 0/ 50 0% 0% NA 1/ 50 2% 2.4% 731 2/ 50 4% 4.8% 731 6/ 50 12% 13.4% 582 5Weight of Evidence is either strong, moderate or weak; a strong weight of evidence is defined as having several studies which support the proposed mode of action, preferably from multiple laboratories with limited evidence of contradiction. Weak evidence is normally defined as a single study from a single laboratory or with a significant amount of contradiction in the literature between reports.

6Specificity to the proposed mode of action. Specificity is high if an event is unique to this particular mode of action. Specificity is low if the event may be seen in many other modes of action.

7This step is confirmed by recent research in mice ( Green et al., 2002; Poet et al., 2003) but has not been investigated in rats, which do not develop forestomach tumors following EGBE exposure.

AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 11 Table 2  Concordance Table Showing the Relationship of Proposed Mode of Action for Formation of Forestomach Tumors in Female Mice to Humans Event Relation to Animal Tumors Overall Weight of Evidence5 Qualitative Relation to Humans Quantitative Relation to Humans Specificity6 Dose/ Temporal Relation Biological plausibility 1. Deposition of EGBE/ BAA in stomach and forestomach via consumption or reingestion of EGBE laden mucous, salivary excretions and fur material Moderate7 Lower/ Earlier Moderate Strong Moderate Moderate 2. Retention of EGBE/ BAA in food particles of the forestomach long after being cleared from other organs Moderate4 Lower/ Earlier Moderate Moderate Low Not Likely 3. Metabolism of EGBE to BAA systemically and in forestomach High Lower/ Earlier High Strong ?? ??

4. Irritation of target cells leading to hyperplasia and ulceration High Lower/ Earlier High Moderate Not Likely Not Likely 5. Continued injury and degeneration leading to high cell proliferation and turnover High ?? High Weak Not Likely Not Likely 6. High cell proliferation and turnover leads to clonal growth of initiated forestomach cells Moderate ?? High Moderate Not Likely Not Likely 8Poly 3 test estimate taken from NTP, 2000 technical report series 484 AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 12 Table 3  Key Tumors Observed in Male Mice Exposed to EGBE ( NTP, 2000)

Control 62.5 ppm 125 ppm 250 ppm Hemangiosarcomas  All organs Overall rate Rate adjusted for intercurrent mortality8 First Incidence ( days) 1/ 50 2% 2.2% 729 1/ 50 2% 2.1% 670 2/ 50 4% 5.0% 704 5/ 50 10% 12.4% 454 Hemangiosarcomas  Liver only Overall rate Rate adjusted for intercurrent mortality First Incidence ( days) 0/ 50 0% 0% NA 1/ 50 2% 2.1% 670 2/ 49 4% 5.0% 704 4/ 49 8% 10% 454 Hemangiosarcomas/ hemangiomas  All organs Overall rate Rate adjusted for intercurrent mortality First Incidence ( days) 1/ 50 2% 2.2% NA 1/ 50 2% 2.1% 670 4/ 50 8% 10% 704 5/ 50 10% 12.4% 454 Hepatocellular Carcinoma Overall rate Rate adjusted for intercurrent mortality First Incidence ( days) 10/ 50 20% 20.8% 374 11/ 50 22% 22.9% 621 16/ 49 33% 35.9% 430 21/ 49 43% 45.9% 312 Hepatocellular Adenoma or Carcinoma Overall rate Rate adjusted for intercurrent mortality First Incidence ( days) 30/ 50 60% 61.9% 374 24/ 50 48% 48.9% 549 31/ 49 63% 67.5% 430 30/ 49 61% 64.8% 312 9Event, weight of evidence and specificity columns were adopted from Klaunig and Kamendulis ( 2003)

10EGBE is metabolized to BAA in rats and mice, but the tumor is only increased in male mice.

11Hemolysis is observed in both sexes of rats and mice, but the tumor is only increased in male mice.

12Hemosiderin is observed in Kupffer cells of both sexes of rats and mice, but the tumor is only increased in male mice. Early ( subchronic) hemosiderin buildup is only observed in male mice, however.

13These effects have been observed to be more pronounced in mice ( Siesky et al, 2002), which are also more susceptible to EGBE induced liver tumor formation than rats ( NTP, 2000).

AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 13 Table 4  Concordance Table Showing the Relationship of Proposed Mode of Action for Formation of Liver Hemangiosarcomas & Hepatocellular Carcinomas in Male Mice to Humans9 Event Relation to Animal Tumors Overall Weight of Evidence5 Qualitative Relation to Humans Quantitative Relation to Humans Specificity6 Dose/ Temporal Relation Biological Plausibility 1. EGBE metabolism to BAA by alcohol dehydrogenase High Lower/ Earlier Moderate Moderate to Strong10 High Moderate 2. RBC hemolysis by BAA High for Hemolysis Lower/ Earlier Moderate Moderate to Strong11 Low Not Likely 3. Buildup of Hemosiderin in Kupffer cells of liver Low Lower/ Earlier Moderate Moderate to Strong12 Not Likely Not Likely 4a. Production of reactive oxygen species by Fenton or Haber Weiss reactions Low Higher/ Earlier High Weak13 Not Likely Not Likely 4b. Kupffer cells activated and release cytokine Low ?? Moderate Weak Not Likely Not Likely 5. Reactive oxygen species results in oxidative DNA damage to endothelial cells Low Higher/ Earlier High Weak12 Not Likely Not Likely 6. Modulation of endothelial cell gene expression Low ?? Moderate Weak Not Likely Not Likely 7. Endothelial cell proliferation Low ?? Moderate Strong Not Likely Not Likely 8. Promotion of initiated endothelial cells Low ?? High Weak Not Likely Not Likely 9. Neoplasm formation Low ?? High Strong Not Likely Not Likely AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 14 REFERENCES Cantox Environmental Inc. ( 2000) EGBE: review of the relevance of forestomach lesions in the female B6C3F1 mouse. Final report; October.

Carpenter, CP; Pozzani, UC; Wiel, CS; et al. ( 1956) The toxicity of butyl cellosolve solvent. AMA Arch Ind Health 14: 114 131.

Commonwealth of Australia. ( 1996) 2 Butoxyethanol. Priority existing chemical number 6. Canberra: Australian Government Publishing Service. Available: http:// www. nicnas. gov. au/ publications/ car/ pec/ pecindex. htm [ 27 January, 2003].

Corley, R. A.; Markham, D. A.; Banks, C.; Delorme, P.; Masterman, A.; Houle, J. M. ( 1997) Physiologically based pharmacokinetics and the dermal absorption of 2 butoxyethanol vapors by humans. Fundam. Appl. Toxicol. 39: 120 130.

Elliot, B. M. and Ashby, J. ( 1997) Review of the genotoxicity of 2 butoxyethanol. Mutat. Res. 387: 89 96.

Green, T.; Toghill, A.; Lee, R.; Moore, R.; Foster, J. ( 2002) The development of forestomach tumors in the mouse following exposure to 2 butoxyethanol by inhalation. Studies on the mode of action and relevance to humans. Toxicology 180: 257 273.

Grice, H. C. ( 1988) Safety evaluation of butylated hydroxyanisole from the perspective of effects on forestomach and oesophageal squamous epithelium. Food Chem. Toxicol. 26: 717 723.

Klaunig, J. E. ( 2002) Mode of action of butoxyethanol for liver hemangiosarcomas in the male mouse. Washington, DC: Presented to U. S. Environmental Protection Agency, National Center for Environmental Assessment; December 3.

Klaunig, J. E. and Kamendulis, L. M. ( 2003) Mode Of Action Of Butoxyethanol Induced Mouse Liver Hemangiosarcomas And Hepatocellular Carcinomas. Tox. Letters. ( Submitted).

National Toxicology Program ( NTP). ( 1998) Toxicology and carcinogenesis studies of 2 butoxyethanol ( CAS no. 111 76 2) in F344/ N rats and B6C3F1 mice ( inhalation studies). Washington, DC: U. S. Department of Health and Human Services, National Institutes of Health. ( National Toxicology Program technical report series no. 484; NIH draft publication no. 98 3974)

National Toxicology Program ( NTP). ( 2000) Toxicology and carcinogenesis studies of 2 butoxyethanol ( CAS no. 111 76 2) in F344/ N rats and B6C3F1 mice ( inhalation studies). Washington, DC: U. S. Department of Health and Human Services, National Institutes of Health. ( National Toxicology Program technical report series no. 484). AUGUST, 2003 INTERIM FINAL  DO NOT CITE OR QUOTE 15 NTP ( 2002). NTP Historical Control Information for the NIH 07 Diet. Available at http:// ehp. niehs. nih. gov/ ntp/ docs/ ntp_ hcrs. html. Updated 25 March, 2002.

Poet, T. S.; Soelberg, J. J.; Weitz, K. K.; Mast, T. J.; Miller, R. A.; Thrall, B. D.; Corley, R. A. ( 2003) Mode of action and pharmacokinetic studies of 2 butoxyethanol in the mouse with an emphasis on forestomach dosimetry. Toxicol. Sci. 71: 176 189.

Siesky, A. M.; Kamendulis, L. M.; Klaunig, J. E. ( 2002) Hepatic effects of 2 butoxyethanol in rodents. Toxicol. Sci. 70: 252 260.

Udden, M. M. ( 1994) Hemolysis and decreased deformability of erythrocytes exposed to butoxyacetic acid, a metabolite of 2 butoxyethanol: II. Resistance in red blood cells from humans with potential susceptibility. J. Appl. Toxicol. 14: 97 102.

Udden, M. M. ( 1995) Effects of butoxyacetic acid on human red cells. Occup. Hyg. 2: 283 292.

Udden, M. M. ( 2002) In vitro sub hemolytic effects of butoxyethanol acid on human and rat erythrocytes. Toxicol. Sci. 69: 258 264.

U. S. Environmental Protection Agency ( 1986) Guidelines for carcinogen risk assessment. Federal Register 51: 33992 34003.

U. S. Environmental Protection Agency ( 1996) Proposed guidelines for carcinogen risk assessment. Washington, DC: Office of Research and Development; report no. EPA/ 600/ P 92/ 003C. Available: http:// www. epa. gov/ ORD/ WebPubs/ carcinogen/ [ 27 January, 2003].

U. S. Environmental Protection Agency. ( 1999a) Ethylene glycol monobutyl ether ( EGBE)( 2 butoxyethanol) ( CASRN 111 76 2). Cincinnati, OH: Office of Health and Environmental Assessment, Environmental Criteria and Assessment Office. Available: http:// www. epa. gov/ iris/ subst/ 0500. htm [ 27 January, 2003].

U. S. Environmental Protection Agency. ( 1999b) Guidelines for carcinogen risk assessment [ draft]. Washington, DC: Risk Assessment Forum; report no. NCEA F 0644. Available: http:// www. epa. gov/ ncea/ raf/ pdfs/ cancer_ gls. pdf.

U. S. Environmental Protection Agency. ( 2003) Draft Final Guidelines for Carcinogen Risk Assessment ( External Review Draft, February 2003). Other Ncea F 0644a. 03 Mar 2003. U. S. Environmental Protection Agency, Risk Assessment Forum, Washington, DC, 125 pp. Available: http:// cfpub. epa. gov/ ncea/ cfm/ recordisplay. cfm? deid= 55445.


[Federal Register Volume 86, Number 94 (Tuesday, May 18, 2021)]
[Proposed Rules]
[Pages 26861-26862]
[FR Doc No: 2021-10368]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

14 CFR Part 71

[Docket No. FAA-2021-0328; Airspace Docket No. 21-ASO-5]
RIN 2120-AA66

Proposed Amendment of Class D and Class E Airspace; Savannah, GA

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Notice of proposed rulemaking (NPRM).

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SUMMARY: This action proposes to amend Class D airspace by removing
unnecessary verbiage from the description, and Class E surface airspace
in Savannah, GA, by updating the dividing line between Savannah/Hilton
Head International Airport and Hunter Army Airfield. Controlled
airspace is necessary for the safety and management of instrument
flight rules (IFR) operations in the area.

DATES: Comments must be received on or before July 2, 2021.

ADDRESSES: Send comments on this proposal to: The U.S. Department of
Transportation, Docket Operations, 1200 New Jersey Avenue SE, West
Building Ground Floor, Room W12-140, Washington, DC 20590-0001;
Telephone:<PHONE_NUMBER>, or<PHONE_NUMBER>. You must identify the
Docket No. FAA-2021-0328; Airspace Docket No. 21-ASO-5, at the
beginning of your comments. You may also submit comments through the
internet at https://www.regulations.gov.
    FAA Order 7400.11E, Airspace Designations and Reporting Points, and
subsequent amendments can be viewed online at https://www.faa.gov/air_traffic/publications/. For further information, you can contact the
Airspace Policy Group, Federal Aviation Administration, 800
Independence Avenue SW, Washington, DC, 20591; telephone: (202) 267-
8783. The Order is also available for inspection at the National
Archives and Records Administration (NARA). For information on the
availability of FAA Order 7400.11E at NARA, email<EMAIL_ADDRESS>or go to https://www.archives.gov/federal-register/cfr/ibr-locations.html.

FOR FURTHER INFORMATION CONTACT: John Fornito, Operations Support
Group, Eastern Service Center, Federal Aviation Administration, 1701
Columbia Avenue, College Park, GA 30337; telephone<PHONE_NUMBER>.

SUPPLEMENTARY INFORMATION:

Authority for This Rulemaking

    The FAA's authority to issue rules regarding aviation safety is
found in Title 49 of the United States Code. Subtitle I, Section 106,
describes the authority of the FAA Administrator. Subtitle VII,
Aviation Programs, describes in more detail the scope of the agency's
authority. This rulemaking is promulgated under the authority described
in Subtitle VII, Part A, Subpart I, Section 40103. Under that section,
the FAA is charged with prescribing regulations to assign the use of
airspace necessary to ensure the safety of aircraft and the efficient
use of airspace. This regulation is within the scope of that authority
as it would amend Class D and E airspace in Savannah, GA.

Comments Invited

    Interested persons are invited to comment on this proposed
rulemaking by submitting such written data, views, or arguments, as
they may desire. Comments that provide the factual basis supporting the
views and suggestions presented are particularly helpful in developing
reasoned regulatory decisions on the proposal. Comments are
specifically invited on the overall regulatory, aeronautical, economic,
environmental, and energy-related aspects of the proposal.
    Communications should identify both docket numbers (Docket No. FAA-
2021-0328 and Airspace Docket No. 21-ASO-5) and be submitted in
triplicate to DOT Docket Operations (see ADDRESSES section for the
address and phone number). You may also submit comments through the
internet at https://www.regulations.gov.
    Persons wishing the FAA to acknowledge receipt of their comments on
this action must submit with those comments a self-addressed stamped
postcard on which the following statement is made: ``Comments to FAA
Docket No. FAA-2020-0328 Airspace Docket No. 21-ASO-5.'' The postcard
will be date/time stamped and returned to the commenter.
    All communications received before the specified closing date for
comments will be considered before taking action on the proposed rule.
The proposal contained in this document may be changed in light of the
comments received. All comments submitted will be available for
examination in the public docket both before and after the comment
closing date. A report summarizing each substantive public contact with
FAA personnel concerned with this rulemaking will be filed in the
docket.

Availability of NPRMs

    An electronic copy of this document may be downloaded through the
internet at http://www.regulations.gov. Recently published rulemaking
documents can also be accessed through the FAA's web page at https://www.faa.gov/air_traffic/publications/airspace_amendments/.
    You may review the public docket containing the proposal, any
comments received and any final disposition in person in the Dockets
Office (see the ADDRESSES section for address and phone number) between
9:00 a.m. and 5:00 p.m., Monday through Friday,

except federal holidays. An informal docket may also be examined
between 8:00 a.m. and 4:30 p.m., Monday through Friday, except federal
holidays at the office of the Eastern Service Center, Federal Aviation
Administration, Room 350, 1701 Columbia Avenue, College Park, GA 30337.

Availability and Summary of Documents for Incorporation by Reference

    This document proposes to amend FAA Order 7400.11E, Airspace
Designations and Reporting Points, dated July 21, 2020, and effective
September 15, 2020. FAA Order 7400.11E is publicly available as listed
in the ADDRESSES section of this document. FAA Order 7400.11E lists
Class A, B, C, D, and E airspace areas, air traffic service routes, and
reporting points.

The Proposal

    The FAA proposes an amendment to 14 CFR part 71 to amend Class D
airspace by removing (previously called Airport/Facility Directory)
from the description, as it is unnecessary, and Class E surface
airspace in Savannah, GA by updating the dividing line separating the
airspace between Savannah/Hilton Head International Airport and Hunter
AAF.
    Class D and E airspace designations are published in Paragraphs
5000, and 6002, respectively, of FAA Order 7400.11E, dated July 21,
2020, and effective September 15, 2020, which is incorporated by
reference in 14 CFR 71.1. The Class E airspace designation listed in
this document will be published subsequently in the Order.
    FAA Order 7400.11, Airspace Designations and Reporting Points, is
published yearly and effective on September 15.

Regulatory Notices and Analyses

    The FAA has determined that this proposed regulation only involves
an established body of technical regulations for which frequent and
routine amendments are necessary to keep them operationally current.
It, therefore: (1) Is not a ``significant regulatory action'' under
Executive Order 12866; (2) is not a ``significant rule'' under DOT
Regulatory Policies and Procedures (44 FR 11034; February 26, 1979);
and (3) does not warrant preparation of a Regulatory Evaluation as the
anticipated impact is minimal. Since this is a routine matter that will
only affect air traffic procedures and air navigation, it is certified
that this proposed rule, when promulgated, will not have a significant
economic impact on a substantial number of small entities under the
criteria of the Regulatory Flexibility Act.

Environmental Review

    This proposal will be subject to an environmental analysis in
accordance with FAA Order 1050.1F, ``Environmental Impacts: Policies
and Procedures'' prior to any FAA final regulatory action.

List of Subjects in 14 CFR Part 71

    Airspace, Incorporation by reference, Navigation (air).

The Proposed Amendment

    In consideration of the foregoing, the Federal Aviation
Administration proposes to amend 14 CFR part 71 as follows:

PART 71--DESIGNATION OF CLASS A, B, C, D, AND E AIRSPACE AREAS; AIR
TRAFFIC SERVICE ROUTES; AND REPORTING POINTS

0
1. The authority citation for part 71 continues to read as follows:

    Authority: 49 U.S.C. 106(f), 106(g); 40103, 40113, 40120; E.O.
10854, 24 FR 9565, 3 CFR, 1959-1963 Comp., p. 389.

Sec.  71.1   [Amended]

0
2. The incorporation by reference in 14 CFR 71.1 of FAA Order 7400.11E,
Airspace Designations and Reporting Points, dated July 21, 2020, and
effective September 15, 2020, is amended as follows:

Paragraph 5000 Class D Airspace.

* * * * *

ASO GA D Savannah, GA [Amended]

Hunter AAF, GA
    (Lat. 32[deg]00'36'' N, long. 81[deg]08'46'' W)
Savannah/Hilton Head International Airport
    (Lat. 32[deg]07'39'' N, long. 81[deg]12'08'' W)

    That airspace extending upward from the surface to and including
2,500 feet MSL within a 4.5-mile radius of Hunter AAF; excluding
that portion of the overlying Savannah, GA, Class C airspace area
and that airspace north of lat. 32[deg]02'30'' N. This Class D
airspace is effective during the specific dates and times
established in advance by a Notice to Airmen. The effective date and
time will thereafter be continuously published in the Chart
Supplement.

Paragraph 6002 Class E Surface Airspace.

* * * * *

ASO GA E2 Savannah, GA [Amended]

Savannah/Hilton Head International Airport, GA
    (Lat. 32[deg]07'39'' N, long. 81[deg]12'08'' W)
Hunter AAF
    (Lat. 32[deg]00'36'' N, long. 81[deg]08'46'' W)

    That airspace extending upward from the surface within a 5-mile
radius of Savannah/Hilton Head International Airport and within a
4.5-mile radius of Hunter AAF, excluding that airspace north of lat.
32[deg]02'30'' N. This Class E airspace area is effective during the
specific dates and times established in advance by a Notice to
Airmen. The effective date and time will thereafter be continuously
published in the Chart Supplement.

    Issued in College Park, Georgia, on May 11, 2021.
Andreese C. Davis,
Manager, Airspace & Procedures Team South, Eastern Service Center, Air
Traffic Organization.
[FR Doc. 2021-10368 Filed 5-17-21; 8:45 am]
BILLING CODE 4910-13-P


[Federal Register: November 20, 2007 (Volume 72, Number 223)]
[Rules and Regulations]
[Page 65221-65224]
[DOCID:fr20no07-4]

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

14 CFR Part 39

[Docket No. FAA-2007-0179; Directorate Identifier 2007-SW-36-AD;
Amendment 39-15264; AD 2007-19-52]
RIN 2120-AA64

Airworthiness Directives; Bell Helicopter Textron Canada Limited
Model 206A, 206B, 206L, 206L-1, 206L-3, 206L-4, 222, 222B, 222U, 230,
407, 427, and 430 Helicopters

AGENCY: Federal Aviation Administration, DOT.

ACTION: Final rule; request for comments.

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SUMMARY: This document publishes in the Federal Register an amendment
adopting Airworthiness Directive (AD) 2007-19-52, which was sent
previously to all known U.S. owners and operators of the specified Bell
Helicopter Textron Canada Limited (BHTC) model helicopters by
individual letters. This AD requires replacing each affected tail

rotor blade (blade) with an airworthy blade with a serial number not
listed in the Rotor Blades, Inc. (RBI), attachment to the BHTC Alert
Service Bulletin (ASB), listed in the applicability section of this AD.
This amendment is prompted by three incidents in which blade tip
weights were slung from blades during flight causing significant
vibration. The actions specified are intended to prevent loss of a
blade tip weight, loss of a blade, and subsequent loss of control of
the helicopter.

DATES: Effective December 5, 2007, to all persons except those persons
to whom it was made immediately effective by Emergency AD 2007-19-52,
issued on September 14, 2007, which contained the requirements of this
amendment.
    The incorporation by reference of certain publications listed in
the regulations is approved by the Director of the Federal Register as
of December 5, 2007.
    Comments for inclusion in the Rules Docket must be received on or
before January 22, 2008.

ADDRESSES: Use one of the following addresses to submit comments on
this AD:
     Federal eRulemaking Portal: Go to http://www.regulations.gov.
 Follow the instructions for submitting comments.

     Fax:<PHONE_NUMBER>.
     Mail: U.S. Department of Transportation, Docket
Operations, M-30, West Building Ground Floor, Room W12-140, 1200 New
Jersey Avenue, SE., Washington, DC 20590.
     Hand Delivery: U.S. Department of Transportation, Docket
Operations, M-30, West Building Ground Floor, Room W12-140, 1200 New
Jersey Avenue, SE., Washington, DC 20590, between 9 a.m. and 5 p.m.,
Monday through Friday, except Federal holidays.
    You may get the service information identified in this AD from Bell
Helicopter Textron Canada, 12,800 Rue de l'Avenir, Mirabel, Quebec
J7J1R4, telephone<PHONE_NUMBER> or<PHONE_NUMBER>, fax<PHONE_NUMBER>.
    Examining the Docket: You may examine the AD docket on the Internet
at http://www.regulations.gov; or in person at the Docket Management

Facility between 9 a.m. and 5 p.m., Monday through Friday, except
Federal holidays. The AD docket contains this AD, the economic
evaluation, any comments received, and other information. The street
address for the Docket Office (telephone<PHONE_NUMBER>) is in the
ADDRESSES section. Comments will be available in the AD docket shortly
after receipt.

FOR FURTHER INFORMATION CONTACT: Sharon Miles, Aviation Safety
Engineer, FAA, Rotorcraft Directorate, Regulations and Guidance Group,
Fort Worth, Texas 76193-0111, telephone<PHONE_NUMBER>, fax (817) 222-
5961.

SUPPLEMENTARY INFORMATION: On September 14, 2007, the FAA issued
Emergency AD 2007-19-52 for the specified BHTC model helicopters, which
requires replacing each affected part-numbered and serial-numbered
blade with an airworthy blade with a serial number not listed in the
RBI attachment to the BHTC ASB, listed in the applicability section of
this AD. That action was prompted by three incidents in which blade tip
weights were slung from the blades during flight causing significant
vibration. The failures have occurred on blades being returned to
service from RBI, from as short as 12 minutes since repair to as long
as 400 hours time-in-service. An investigation indicates that the tip
weights were missing the adhesive that should have been applied during
the weight-and-balance process on these blades. This condition, if not
corrected, could result in loss of a blade tip weight, loss of a blade,
and subsequent loss of control of the helicopter.
    Transport Canada, the airworthiness authority for Canada, notified
the FAA that an unsafe condition may exist on these helicopter models.
Transport Canada advises of three reports of balance weights departing
from the blades during flight. They also advise that they determined in
the investigation that the unsafe condition results from the loss of
the tip weights and that the failure can occur at any time.
    BHTC has issued the following Alert Service Bulletins (ASBs):
     No. 206-07-116, dated September 11, 2007, for BHTC Model
206 A/B series helicopters;
     No. 206L-07-148, dated September 11, 2007, for BHTC Model
206L series helicopters;
     No. 222-07-106, Revision A, dated September 13, 2007, for
BHTC Model 222 and 222B helicopters;
     No. 222U-07-77, Revision A, dated September 13, 2007, for
BHTC Model 222U helicopters;
     No. 230-07-38, Revision A, dated September 13, 2007, for
BHTC Model 230 helicopters;
     No. 407-07-81, dated September 11, 2007, for BHTC Model
407 helicopters;
     No. 427-07-18, dated September 11, 2007, for BHTC Model
427 helicopters; and
     No. 430-07-41, Revision A, dated September 13, 2007, for
BHTC Model 430 helicopters.
    All of the ASBs contain a letter from RBI indicating that certain
blades processed by RBI may be missing the adhesive applied to the tip
weight screws during the weight and balance process. Transport Canada
classified the ASBs as mandatory and issued AD No. CF-2007-21, dated
September 13, 2007, to ensure the continued airworthiness of these
helicopters in Canada.
    Paragraph (a) of the AD states that you must replace any affected
blade with an airworthy blade with a serial number not listed in the
applicability section of this AD. The serial numbers are not directly
listed in the applicability section of this AD. The ASBs for the
various model helicopters are listed in the applicability section. The
affected part and serial numbers are listed in the RBI attachment to
each of the BHTC ASBs listed in the applicability section of this AD.
We have clarified that language in the AD and have determined that this
change will neither increase the economic burden on any operator nor
increase the scope of the AD.
    These helicopter models are manufactured in Canada and are type
certificated for operation in the United States under the provisions of
14 CFR 21.29 and the applicable bilateral agreement. Pursuant to the
applicable bilateral agreement, Transport Canada has kept the FAA
informed of the situation described above. The FAA has examined the
findings of Transport Canada, reviewed all available information, and
determined that AD action is necessary for products of these type
designs that are certificated for operation in the United States.
    Since the unsafe condition described is likely to exist or develop
on other BHTC model helicopters of these same type designs, the FAA
issued Emergency AD 2007-19-52 to prevent loss of a blade tip weight,
loss of a blade, and subsequent loss of control of the helicopter. The
AD requires before further flight, removing and replacing each affected
blade with an airworthy blade. The actions must be accomplished for the
blade part numbers with serial numbers listed in the RBI attachment to
the ASBs described previously. The short compliance time involved is
required because the previously described critical unsafe condition can
adversely affect the structural integrity and controllability of the
helicopter. Therefore, removing and replacing each affected blade with
an airworthy blade is required before further flight, and this AD must
be issued immediately.
    Since it was found that immediate corrective action was required,
notice

and opportunity for prior public comment thereon were impracticable and
contrary to the public interest, and good cause existed to make the AD
effective immediately by individual letters issued on September 14,
2007, to all known U.S. owners and operators of the specified BHTC
model helicopters. These conditions still exist, and the AD is hereby
published in the Federal Register as an amendment to 14 CFR 39.13 to
make it effective to all persons.
    The FAA estimates that this AD will affect 3741 helicopters of U.S.
registry, and it will take about 2 hours to determine if a blade is
affected per helicopter at an average labor rate of $80 per work hour.
The ASB contains a warranty statement that owners or operators of Bell
helicopters who comply with the instructions in the ASB will be
eligible to return defective blades identified by serial number in the
compliance section to their nearest RBI facility for inspection and
repair at no cost. Based on these figures, we estimate the total cost
impact of the AD on U.S. operators to be $589,560, assuming all
shipping, inspection, and repair costs are paid by RBI or Bell.

Comments Invited

    This AD is a final rule that involves requirements that affect
flight safety and was not preceded by notice and an opportunity for
public comment; however, we invite you to submit any written data,
views, or arguments regarding this AD. Send your comments to an address
listed under ADDRESSES. Include ``Docket No. FAA-2007-0179; Directorate
Identifier 2007-SW-36-AD'' at the beginning of your comments. We
specifically invite comments on the overall regulatory, economic,
environmental, and energy aspects of the AD. We will consider all
comments received by the closing date and may amend the AD in light of
those comments.
    We will post all comments we receive, without change, to http://www.regulations.gov
, including any personal information you provide. We

will also post a report summarizing each substantive verbal contact
with FAA personnel concerning this AD. Using the search function of the
docket web site, you can find and read the comments to any of our
dockets, including the name of the individual who sent the comment. You
may review the DOT's complete Privacy Act Statement in the Federal
Register published on April 11, 2000 (65 FR 19477-78).

Regulatory Findings

    We have determined that this AD will not have federalism
implications under Executive Order 13132. This AD will not have a
substantial direct effect on the States, on the relationship between
the national Government and the States, or on the distribution of power
and responsibilities among the various levels of government.
    For the reasons discussed above, I certify that the regulation:
    1. Is not a ``significant regulatory action'' under Executive Order
12866;
    2. Is not a ``significant rule'' under the DOT Regulatory Policies
and Procedures (44 FR 11034, February 26, 1979); and
    3. Will not have a significant economic impact, positive or
negative, on a substantial number of small entities under the criteria
of the Regulatory Flexibility Act.
    We prepared an economic evaluation of the estimated costs to comply
with this AD. See the AD docket to examine the economic evaluation.

Authority for This Rulemaking

    Title 49 of the United States Code specifies the FAA's authority to
issue rules on aviation safety. Subtitle I, Section 106, describes the
authority of the FAA Administrator. Subtitle VII, Aviation Programs,
describes in more detail the scope of the Agency's authority.
    We are issuing this rulemaking under the authority described in
Subtitle VII, Part A, Subpart III, Section 44701, ``General
requirements.'' Under that section, Congress charges the FAA with
promoting safe flight of civil aircraft in air commerce by prescribing
regulations for practices, methods, and procedures the Administrator
finds necessary for safety in air commerce. This regulation is within
the scope of that authority because it addresses an unsafe condition
that is likely to exist or develop on products identified in this
rulemaking action.

List of Subjects in 14 CFR Part 39

    Air transportation, Aircraft, Aviation safety, Incorporation by
reference, Safety.

Adoption of the Amendment

0
Accordingly, pursuant to the authority delegated to me by the
Administrator, the Federal Aviation Administration amends part 39 of
the Federal Aviation Regulations (14 CFR part 39) as follows:

PART 39--AIRWORTHINESS DIRECTIVES

0
1. The authority citation for part 39 continues to read as follows:

    Authority: 49 U.S.C. 106(g), 40113, 44701.

Sec.  39.13  [Amended]

0
2. Section 39.13 is amended by adding a new airworthiness directive to
read as follows:

2007-19-52 Bell Helicopter Textron Canada Limited: Amendment 39-
15264. Docket No. FAA-2007-0179; Directorate Identifier 2007-SW-36-
AD.

    Applicability: Model 206A, 206B, 206L, 206L-1, 206L-3, 206L-4,
222, 222B, 222U, 230, 407, 427, and 430 helicopters, with a tail
rotor blade (blade) having a part number and serial number as listed
in the following Bell Helicopter Textron Alert Service Bulletins
(ASBs), installed, certificated in any category.

----------------------------------------------------------------------------------------------------------------
             ASB No.                    Revision               Date                   Helicopter model
----------------------------------------------------------------------------------------------------------------
206-07-116......................  ....................  September 11, 2007  206A and 206B.
206L-07-148.....................  ....................  September 11, 2007  206L, L-1, L-3, and L-4.
222-07-106......................  A...................  September 13, 2007  222 and 222B.
222U-07-77......................  A...................  September 13, 2007  222U.
230-07-38.......................  A...................  September 13, 2007  230.
407-07-81.......................  ....................  September 11, 2007  407.
427-07-18.......................  ....................  September 11, 2007  427.
430-07-41.......................  A...................  September 13, 2007  430.
----------------------------------------------------------------------------------------------------------------

    Compliance: Required as indicated, unless accomplished
previously.
    To prevent loss of a blade tip weight, loss of a blade, and
subsequent loss of control of the helicopter, accomplish the
following:
    (a) Before further flight, replace any affected blade with an
airworthy blade with a serial number not listed in the Rotor Blade,
Inc. (RBI), attachment to an ASB listed in the applicability section
of this AD.
    (b) To request a different method of compliance or a different
compliance time for this AD, follow the procedures in 14 CFR 39.19.
Contact the Manager, Regulations and Guidance Group, FAA, ATTN:
Sharon Miles,

Fort Worth, Texas 76193-0111, telephone<PHONE_NUMBER>, fax (817)
222-5961, for information about previously approved alternative
methods of compliance.
    (c) Special flight permits will not be issued.
    (d) Each affected blade is identified by serial number as listed
in the Rotor Blade, Inc., letter attached to Bell Helicopter Textron
Alert Service Bulletin (ASB) Nos. 206-07-116, 206L-07-148, 407-07-
81, and 427-07-18, all dated September 11, 2007; and ASB Nos. 222-
07-106, 222U-07-77, 230-07-38, and 430-07-41, all Revision A, all
dated September 13, 2007. The Director of the Federal Register
approved this incorporation by reference in accordance with 5 U.S.C.
552(a) and 1 CFR part 51. Copies may be obtained from Bell
Helicopter Textron Canada, 12,800 Rue de l'Avenir, Mirabel, Quebec
J7J1R4, telephone<PHONE_NUMBER> or<PHONE_NUMBER>, fax (450) 433-
0272. Copies may be inspected at the FAA, Office of the Regional
Counsel, Southwest Region, 2601 Meacham Blvd., Room 663, Fort Worth,
Texas or at the National Archives and Records Administration (NARA).
For information on the availability of this material at NARA, call
202-741-6030, or go to: http://www.archives.gov/federal_register/code_of_federal_regulations/ibr_locations.html
.

    Note: The subject of this AD is addressed in Transport Canada
(Canada) AD No. CF-2007-21, dated September 13, 2007.
    (e) This amendment becomes effective on December 5, 2007, to all
persons except those persons to whom it was made immediately
effective by Emergency AD 2007-19-52, issued September 14, 2007,
which contained the requirements of this amendment.

    Issued in Fort Worth, Texas, on October 31, 2007.
David A. Downey,
Manager, Rotorcraft Directorate, Aircraft Certification Service.
[FR Doc. E7-22416 Filed 11-19-07; 8:45 am]

BILLING CODE 4910-13-P


[Federal Register Volume 87, Number 55 (Tuesday, March 22, 2022)]
[Notices]
[Page 16306]
[FR Doc No: 2022-06011]

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DEPARTMENT OF TRANSPORTATION

Federal Railroad Administration

[Docket Number FRA-2022-0018]

Petition for Waiver of Compliance and Statutory Exemption

    Under part 211 of title 49 Code of Federal Regulations (CFR), this
document provides the public notice that on February 24, 2022, Canadian
Pacific Railway (CP) and Union Pacific Railroad Company (UP) jointly
petitioned the Federal Railroad Administration (FRA) for a waiver of
compliance from certain provisions of the Federal railroad safety
regulations contained at 49 CFR part 232 (Brake System Safety Standards
for Freight and Other Non-Passenger Trains and Equipment; End-of-Train
Devices). CP and UP also request an exemption from the requirements of
title 49, United States Code (U.S.C.), section 20303, which states that
a rail vehicle with defective or insecure equipment may be moved when
necessary to make repairs to the nearest available place at which the
repairs can be made. See 49 U.S.C. 20306. FRA assigned the petition
Docket Number FRA-2022-0018.
    Specifically, CP and UP request relief from 49 CFR 232.213,
Extended haul trains; 232.15, Movement of defective equipment; and
232.103(f), General requirements for all train brake systems, and an
exemption from the requirements of 49 U.S.C. 20303, for a potash unit
train pair (CP train symbols 668 and 669), which are designated as
extended haul trains, that operate between loading facilities in
Saskatchewan, Canada, and the ports of Portland, Oregon, United States.
The requested relief would allow technology-based advanced testing (the
Automated Brake Effectiveness (ABE) Test Process) performed by wheel
temperature detectors as an alternative approach to manual Class I
brake tests performed by Certified Car Inspectors (Qualified Mechanical
Inspectors). The tests would take place on westbound CP symbol 669
trains at the designated inspection location in Lethbridge, Alberta,
Canada. The petitioners state that the ABE Test Process is expected to
provide more accurate brake testing, more proactive identification and
repair of defects, and safer railway operations.
    Petitioners also explain that on December 10, 2021, Transport
Canada granted two exemptions to CP under the Canadian Railway Safety
Act that permit the use of CP's Remote Safety Inspection Process (RSIP)
and ABE Test Process as alternative practices to meet certain freight
car safety and air brake inspections performed in Canada as required by
Canadian rules. The ABE Test Process has been in existence in Canada
for over ten years, and FRA has audited the process as part of its
investigation of test waivers under Docket Numbers FRA-2016-0018 and
FRA-2018-0049. FRA believes that the RSIP, by utilizing Certified Car
Inspectors in near real-time oversight of the process, meets the
requirements of Sec.  232.213(a)(3), and does not require relief for
this instance. Petitioners state that the train pair currently receives
and will continue to receive all inspections in Canada by CP employees
prior to interchanging to the UP, and US operations would not change.
    FRA may grant an exemption from the requirements of 49 U.S.C. 20303
only on the basis of (1) evidence developed at a hearing; or (2) an
agreement between national railroad labor representatives and the
developer of the equipment or technology at issue. 49 U.S.C. 20306. FRA
notes that the public hearing FRA previously held to address a similar
request for exemption from UP (Docket Number FRA-2016-0018) addresses
substantially the same issues as this current request. Thus, FRA
believes a separate public hearing on the current request is
unnecessary, and in considering the joint CP and UP request in this
docket, FRA intends to rely on the findings of the hearing conducted in
Docket Number FRA-2016-0018.
    A copy of the petition, as well as any written communications
concerning the petition, is available for review online at
www.regulations.gov.
    Interested parties are invited to participate in these proceedings
by submitting written views, data, or comments.
    All communications concerning these proceedings should identify the
appropriate docket number and may be submitted at http://www.regulations.gov. Follow the online instructions for submitting
comments.
    Communications received by May 23, 2022 will be considered by FRA
before final action is taken. Comments received after that date will be
considered if practicable.
    Anyone can search the electronic form of any written communications
and comments received into any of our dockets by the name of the
individual submitting the comment (or signing the document, if
submitted on behalf of an association, business, labor union, etc.).
Under 5 U.S.C. 553(c), the U.S. Department of Transportation (DOT)
solicits comments from the public to better inform its processes. DOT
posts these comments, without edit, including any personal information
the commenter provides, to www.regulations.gov, as described in the
system of records notice (DOT/ALL-14 FDMS), which can be reviewed at
https://www.transportation.gov/privacy. See also https://www.regulations.gov/privacy-notice for the privacy notice of
regulations.gov.

    Issued in Washington, DC.
John Karl Alexy,
Associate Administrator for Railroad Safety, Chief Safety Officer.
[FR Doc. 2022-06011 Filed 3-21-22; 8:45 am]
BILLING CODE 4910-06-P