HED DOC. NO. 014555 CANCER ASSESSMENT DOCUMENT EVALUATION OF THE CARCINOGENIC POTENTIAL OF OXADIAZON ( THIRD REVIEW)

FINAL REPORT 1 MAY 2001 CANCER ASSESSMENT REVIEW COMMITTEE HEALTH EFFECTS DIVISION OFFICE OF PESTICIDE PROGRAMS Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report ii DATA PRESENTATION: Nancy McCarroll, Toxicologist DOCUMENT PREPARATION: Sanjivani Diwan, Executive Secretary COMMITTEE MEMBERS IN ATTENDANCE: ( Signature indicates concurrence with the assessment unless otherwise stated).

Karl Baetcke William Burnam Kerry Dearfield Vicki Dellarco Yiannakis Ioannou Nancy McCarroll Esther Rinde Joycelyn Stewart Clark Swentzel Linda Taylor NON COMMITTEE MEMBERS IN ATTENDANCE ( Signature indicates concurrence with the pathology report and statistical analysis of data, respectively)

John M. Pletcher Pathology Consultant Lori Brunsman, Statistical Analysis Veronique LaCapra CRM ( SRRD) Seyed Tadayon Chemist ( Chem and Exposure)

_______________________________________________________________________________ Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report iii CONTENTS Executive Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . iv I. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 II. Background Information . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 III. Evaluation of Carcinogenicity Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 1. Combined Chronic Toxicity/ Carcinogenicity Study in Wistar Rats . . . . . . . . . . . . . . . 2 2. Combined Chronic Toxicity/ Carcinogenicity Studies in ICR JCL mice . . . . . . . . . . 8 IV. Other Toxicology Data . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 1. Mutagenicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13 2. Structure Activity Relationships . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15 3. Mode of Action Studies. . . . . . . . . . . . . . . . . . . .. . . . . . . . . . .. . . . . . . . . . . .. . . . . . .17 V. Committee's Assessment of the Weight of the Evidence . . . . . . . . . . . . . . . . . . . . . . . . . . 18 VI. Classification of Carcinogenic Potential . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19 VII. Quantification of Carcinogenic Potential. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20 VIII. Bibliography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report iv EXECUTIVE SUMMARY On March 7, 2001, the Cancer Assessment Review Committee ( CARC) of the Health Effects Division ( HED) of the Office of Pesticide Programs met to reevaluate the carcinogenic potential of oxadiazon.

In the original carcinogenicity assessment, oxadiazon was classified as a Group B2, probable human carcinogen, based on the increased incidence of malignant or combined benign and malignant liver tumors in multiple species ( CD  1 mice and F344 rats of one or both sexes) and in multiple experiments ( two mouse studies and one rat study ( 1984; HED Document No. 004097). On September 3, 1986 during the 2nd meeting, the Toxicology Branch Peer Review Committee reaffirmed the earlier classification of oxadiazon as a Group B2 carcinogen but there was a minority opinion that the agent should be placed in Group C, possible human carcinogen ( 1987; HED Document No. 007798). Based on weight of the evidence for oxadiazon, the Scientific Advisory Panel reiterated the minority view ( 1987; HED Document No. 007798). Subsequently, the cancer classification for oxadiazon was revised to a Group C carcinogen and for the quantification of human cancer risk, a linear low dose extrapolation approach was recommended ( 1987; HED Document No. 007798). The decision to reclassify oxadiazon as a Group C carcinogen was based on the rationale that liver tumors were produced in two of the three positive studies ( one mouse study and one rat study) at doses that exceeded the maximum tolerated dose ( MTD).

At the March 7, 2001 CARC meeting, information/ data previously not available to the Peer Review Committee were considered which included chronic toxicity/ carcinogenicity studies in Wistar rats and ICR JCL mice. In the rat study, oxadiazon was administered in the diet to groups of 80 male and 80 female Wistar rats at concentrations of 0, 3, 10, 100 or 1000 ppm ( 0, 0.106, 0.36, 3.5 or 39 mg/ kg/ day for males and 0, 0.131, 0.44, 4.2 or 44 mg/ kg/ day for females, respectively) for up to 104 weeks. In the mouse study, oxadiazon was administered to groups of 80 male and 80 female ICR JCL mice at dietary concentrations of 0, 3, 10, 100 or 1000 ppm ( 0, 0.315, 1.09, 10.6 or 113 mg/ kg/ day for males and 0, 0.278, 0.92, 9.3 or 99 mg/ kg/ day for females, respectively) for 98/ 99 weeks. The Registrant also submitted mechanistic studies to support the proposed mode of action for liver tumor induction observed in these studies.

The CARC concluded that:

! There was clear evidence that oxadiazon was carcinogenic to male Wistar rats because: 1) There were statistically significant positive trends for liver adenomas, carcinomas and combined adenomas/ carcinomas. There was a statistically significant increase by pair wise comparison with the controls for liver adenomas and combined liver adenomas/ carcinomas at 100 and 1000 ppm and for liver carcinomas at 1000 ppm indicating a malignant component to the liver tumors; and 2) The incidences of liver adenomas at 100 ppm and 1000 ppm and carcinomas at 1000 ppm were outside the published range of spontaneous incidences in Wistar rats ( range: adenomas, 0% 2.5%; carcinomas, 0% 2.5%). The highest dose level tested in this study was considered to be Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report v adequate and not excessive in male rats because there were decreases in body weight gains and the clinical and histopathological liver changes observed were not severely adverse. The survival of the animals was not affected by the treatment. There was a statistically significant increasing trend for liver carcinomas in females but there was no significant increase in liver tumors in treated females by pair wise comparisons with controls. The Committee determined that, for female rats, the highest dose was adequate based on an increased incidence of chronic nephropathy. The CARC concluded that the increased incidence of liver tumors observed in the male rats was treatment related.

! There was clear evidence that oxadiazon was carcinogenic to male and female ICRJCL mice because: There were statistically significant positive trends for liver adenomas, carcinomas and combined adenomas/ carcinomas in both sexes. There were also statistically significant increases by pair wise comparison of the dosed groups with the controls for liver adenomas and carcinomas as well as for combined liver adenomas/ carcinomas at 100 and 1000 ppm for males and at 1000 ppm for females. There was a malignant component to the liver tumors in both sexes. The highest dose level tested was considered to be adequate and not excessive in both sexes based on increased liver weights and histopathological changes in the liver at 1000 ppm which were not severely adverse. The Committee concluded that there were treatment related increases in both benign and malignant liver tumors in male and female mice.

The positive results of an in vitro cell transformation assay are in concordance with the findings of in vivo rodent bioassays.

! A battery of acceptable mutagenicity assays indicated that oxadiazon was not mutagenic.

! The mechanistic studies provide insufficient data to determine whether a threshold mechanism exists for the induction of liver tumors observed in rats and mice. Nevertheless, the formation of brown pigment in the liver and kidneys of rats and mice is consistent with the known inhibitory action of oxadiazon toward protoporphyrinogen oxidase, a critical enzyme in chlorophyll and heme biosynthesis.

In accordance with the EPA Draft Guidelines for Carcinogen Risk Assessment ( July, 1999), the CARC classified oxadiazon into the category " Likely to be carcinogenic to humans" based on the following weight of the evidence considerations:

1. Treatment related benign and malignant liver tumors were observed in two species. There was clear evidence that oxadiazon induced a statistically significant increase in liver tumors in male Wistar rats and male and female ICR JCL mice. The findings of liver tumors are consistent with the results of earlier studies in male F 344 rats and male and female CD mice. The positive results from an in vitro cell transformation assay are in concordance with the results of in vivo rodent bioassays.

2. Oxadiazon was not mutagenic. However, it causes cell transformation in vitro; these results are in concordance with the carcinogenicity seen in in vivo rodent studies. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report vi The Committee recommended a low dose linear extrapolation approach for the quantification of human cancer risk based on the most potent liver tumors in rats and mice. This approach is supported by the inadequacy of data on the mode of action for oxadiazon induced liver tumors in rodents. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 1 I. INTRODUCTION According to the original carcinogenicity assessment for oxadiazon, the pesticide was ranked as a Group B2, probable human carcinogen ( 1984; HED Document No. 004097). The rationale for the classification, Group B2, was based on the increased incidence of malignant or combined malignant and benign liver tumors in multiple species ( CD  1 mice and F344 rats of one or both sexes) and in multiple experiments ( two mouse studies and one rat study). The Toxicology Branch Peer Review of this agent was later held on September 3, 1986 and the Committee affirmed the earlier classification of oxadiazon as a Group B2 carcinogen but there was a minority opinion that the agent should be placed in Group C, possible human carcinogen ( 1987; HED Document No. 007798). Review of the weight of the evidence on oxadiazon by the Scientific Advisory Panel reiterated this minority view ( 1987; HED Document No. 007798). At that time, the Agency's decision on the carcinogenic potential of oxadiazon concurred with the Scientific Advisory Panel's ( SAP) classification of oxadiazon as a Group C carcinogen ( 1987; HED Document No. 007798). The decision to reclassify oxadiazon as a Group C carcinogen was based on the rationale that liver tumors were produced in two of the three positive studies ( one mouse study and one rat study) at doses that exceeded the maximum tolerated dose ( MTD). For the quantification of human cancer risk a linear low dose extrapolation approach was recommended ( Q1*= 1.4 x 10 1( mg/ kg/ day) 1 ).

On March 7, 2001, the Cancer Assessment Review Committee ( CARC) met to reconsider the carcinogenicity classification of oxadiazon under the draft Agency Cancer Risk Assessment Guidelines ( 1999) for the human cancer risk assessment. At this meeting, information/ data previously not available or relevant to this review were presented by Nancy McCarroll of the Toxicology Branch. These include a chronic/ carcinogenicity toxicity study in Wistar rats ( MRID No. 40993401), a carcinogenicity study in ICR JCL mice ( MRID No. 40993301), genetic toxicology as well as mechanistic studies and data on structurally related compounds. Based on the available studies, the quantitative risk to humans was also evaluated.

II. BACKGROUND INFORMATION Oxadiazon ( P. C. Code: 109001, CAS Number: 19666 30 9, 5 tert butyl 4( 2,4 dichloro 5 isopropoxyphenyl) 1,3,4 oxadiazol 2 one), also known as Ronstar, is a selective pre emergent and early post emergence herbicide that is effective primarily for the control of annual grasses and broadleaf weeds in turf. It has no food or feed uses. Aventis CropScience USA is supporting use of oxadiazon on golf courses, ornamentals, apartment/ condo lawns, athletic fields, parks, playgrounds and cemeteries. Oxadiazon destroys cell membranes and inhibits photosynthesis, probably by generating oxidizing radicals in the presence of light and is a powerful inhibitor of plant, yeast and mouse protoporphyrinogen oxidase, an enzyme critical in the biosynthesis of chlorophyll and heme ( Matringe et al., 1989). Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 2 . Figure 1. Chemical Structure of Oxadiazon III. EVALUATION OF CARCINOGENICITY AND OTHER EVIDENCE 4. Previous Chronic Toxicity/ Carcinogenicity Studies Earlier tumor data for Oxadiazon in F 344 rats and CD 1 mice were discussed previously ( HED Document NO. 007798, dated August 27, 1987) and are not reiterated here.

2. Combined Chronic Toxicity/ Carcinogenicity Study in Wistar Rats Reference Y. Shirasu ( 1987). Oxadiazon  24 Month Chronic Toxicity and Carcinogenicity Study in Rats. Institute of Environmental Toxicology, Tokyo, Japan; Study No. Not listed; Report dated February 1987. ( Unpublished) MRID: 40993401 A. Experimental Design Oxadiazon ( 95.9%) was administered to SPF Wistar rats ( 80/ sex/ dose) in the diet at dose levels of 0, 3, 10, 100 or 1000 ppm ( equivalent to 0, 0.106, 0.36, 3.5 or 39 mg/ kg/ day for males or 0, 0.131, 0.44, 4.2 or 44 mg/ kg/ day for females) for 104 weeks. All 80 rats/ sex/ dose were reportedly examined for histopathology.

B. Discussion of Tumor Data Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 3 The incidences of liver tumors in male and female rats are presented in Tables 1 and 2, respectively. For males, there were statistically significant ( p< 0.01) increasing trends for liver adenomas, carcinomas and combined adenomas/ carcinomas ( Table 1). There were also significant increases in the pair wise comparisons with the controls for liver adenomas at 100 ppm ( p< 0.05) and 1000 ppm ( p< 0.01), carcinomas at 1000 ppm ( p< 0.05) and combined adenomas/ carcinomas at 100 ppm ( p< 0.05) and 1000 ppm ( p< 0.01). For female rats, there was a statistically significant increasing trend ( p< 0.05) for liver carcinomas only and no significant increases in pair wise comparisons of the treated groups with the controls were noted for liver adenomas, carcinomas and combined adenomas/ carcinomas ( Table 2).

Historical control data were not provided by the performing laboratory; however, the spontaneous incidences of liver tumors in Wistar rats reported by Welsh and Poteracki ( 1994) are as follows: males adenomas: 1.02%, range 0 2.5%; carcinomas: 0.88%, range 0 2.5%; females adenomas: 2.34%, range 0 12%; carcinomas: 0.88%, range 0 10%. The incidences of adenomas at 100 and 1000 ppm ( 9% and 13% , respectively) and carcinomas ( 10%) at 1000 ppm in males exceeded the range of available spontaneous incidences. The incidences of liver carcinomas ( 4%) in females did not exceed the range of available spontaneous incidences. The Committee concluded that the increase in liver tumors in male rats was treatment related.

C. Non neoplastic Lesions In 1991, the Agency requested the Registrant to provide new pathology summary tables and indicate the exact number of each tissue that was examined ( HED Document No. 008949) because the exact number of tissues/ organs examined could not be verified by the Reviewers. No correspondence regarding this request has been presented to HED. However, the recent review of data by the HED statistician indicated that none of the animals were excluded from the analyses. Therefore, the Committee concluded that the integrity of the study or the interpretation of the results is not compromised by this data deficiency.

The histopatholgical examination revealed increases in non neoplastic changes in the liver at 1000 ppm. These included: centrilobular liver swelling (

and  ) ; acidophilic foci of cellular alteration (

) ; and brown pigmentation in the Stellate cells (

and  ) ( Table 3). At 100 ppm, a significant ( p< 0.05) increase in the number of males with centrilobular liver swelling was seen. Brown pigmentation in the proximal tubular cells (

and  ) and in cortical interstitial tissue (

) as well as chronic nephropathy (  ) were also noted in the kidneys of high dose rats. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 4 Table 1. Oxadiazon  SPF Wistar Rat Study Male Liver Tumor Rates+ and Exact Trend Test and Fisher's Exact Test Results ( p values) ( Brunsman, 2001)

Dose ( ppm)

0 3 10 100 1000 Adenomas (%)

p = 0/ 53 ( 0)

0.001** 1/ 55 ( 2)

0.509 1/ 54 ( 2)

0.505 5a/ 54 ( 9)

0.030* 7a / 52 ( 13)

0.006**

Carcinomas (%)

p= 0/ 53 ( 0)

0.000** 0/ 55 ( 0)

1.000 0/ 54 ( 0)

1.000 0/ 54 ( 0)

1.000 5b/ 52 ( 10)

0.027*

Combined (%)

p = 0/ 53 ( 0)

0.000** 1/ 55 ( 2)

0.509 1/ 54 ( 2)

0.505 5/ 54 ( 9)

0.030* 12/ 52 ( 23)

0.000** + Number of tumor bearing animals/ Number of animals examined, excluding those that died or were sacrificed before week 53. a First adenoma observed simultaneously at week 78 in interim sacrifice animals, doses 100 and 1000 ppm. b First carcinoma observed at week 78 in an interim sacrifice animal, dose 1000 ppm.

Note: 26 and 56 week interim sacrifice animals are not included in this analysis. There were no liver tumors in any interim sacrifice animals at 26 or 52 weeks.

Significance of trend denoted at control.

Significance of pair wise comparison with control denoted at dose level.

If *, then p < 0.05.

If **, then p < 0.01. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 5 Table 2. Oxadiazon  SPF Wistar Rat Study:

Female Liver Tumor Rates+ and Exact Trend Test and Fisher's Exact Test Results ( p values) ( Brunsman, 2001)

Dose ( ppm)

0 3 10 100 1000 Adenomas (%)

p = 1a/ 52 ( 2)

0.550 1/ 52 ( 2)

0.752 1/ 55 ( 2)

0.738 1/ 53 ( 2)

0.748 1/ 55 ( 2)

0.738 Carcinomas (%)

p= 0/ 52 ( 0)

0.042* 0/ 52 ( 0)

1.000 0/ 55 ( 0)

1.000 0/ 53 ( 0)

1.000 2b/ 55 ( 4)

0.262 Combined (%)

p = 1/ 52 ( 2)

0.098 1/ 52 ( 2)

0.752 1/ 55 ( 2)

0.738 1/ 53 ( 2)

0.748 3/ 55 ( 5)

0.330 + Number of tumor bearing animals/ Number of animals examined, excluding those that died or were sacrificed before week 53. a First adenoma observed at week 103, dose 0 ppm. b First carcinoma observed at week 104, dose 1000 ppm Note: 26  and 52 week interim sacrifice animals are not included in this analysis. There were no liver tumors in any in terim sacrifice animals at 26 and 56 weeks. Significance of trend denoted at control.

Significance of pair wise comparison with control denoted at dose level.

If *, then p < 0.05.

If **, then p < 0.01.

Table 3. Non neoplastic Lesions in the Liver of Wistar Rats Fed Dietary Administrations of Oxadiazon for 104 Weeks Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 6 Lesions of the Liver Malesa Group ( ppm) Femalesa Group ( ppm)

0 3 10 100 1000 0 3 10 100 1000 Centrilobular hepatocellular Swelling 1 2 1 8* 52* 3 2 1 9 33**

Foci of Cellular Alteration ( acidophilic) 9 14 14 9 18* 12 10 8 14 9 Brown Pigmentation of Stellate Cells 0 0 0 1 35*** 4 1 4 1 12**

Focal Hepatocellular Fatty Change 3 7 7 10* 8 9 10 3 8 5 a 80 animals/ sex were reportedly examined at each dose level. * Significantly different ( p< 0.05) than the vehicle control by Fisher's Exact Test. ** Significantly different ( p< 0.01) than the vehicle control by Fisher's Exact Test. *** Significantly different ( p< 0.001) than the vehicle control by Fisher's Exact Test.

Selected non neoplastic changes in the kidney, which were considered to be treatment related, are shown in Table 4. At 1000 ppm, these included: brown pigmentation in the proximal tubular cells ( p< 0.001,

 ) , brown pigmentation in the cortical interstitial tissue ( p< 0.001,

) , and chronic nephropathy ( p< 0.01,  ) . At lower doses, non neoplastic lesions were comparable to the vehicle control values.

Table 4. Non neoplastic Lesions in the Kidneys of Wistar Rats Fed Dietary Administrations of Oxadiazon for 104 Weeks Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 7 Lesions of the Kidneys Malesa Group ( ppm) Femalesa Group ( ppm)

0 3 10 100 1000 0 3 10 100 1000 Brown Pigmentation in Proximal Tubular Cells 3 4 1 2 50*** 6 5 8 13 20***

Brown Pigmentation in Cortical Interstitial Tissue 2 0 0 1 49*** 0 0 1 1 2 Chronic Nephropathy 28 28 33 36 37 11 16 15 14 26**

a 80 animals/ sex were reportedly examined at each dose level. * Significantly different ( p< 0.05) than the vehicle control by Fisher's Exact Test. ** Significantly different ( p< 0.01) than the vehicle control by Fisher's Exact Test. *** Significantly different ( p< 0.001) than the vehicle control by Fisher's Exact Test C. Adequacy of Dosing for Assessment of Carcinogenic Potential Statistical evaluation of mortality indicated no significant incremental changes with increasing doses of oxadiazon in the male and female rats ( Brunsman, 2001). The dosing at the highest dose ( 1000 ppm) was considered to be adequate and not excessive in male rats based on decreased body weight gain ( generally throughout the study), signs of transient anemia ( evident at week 26), increased serum enzyme activity ( LDH

 63%; ALP

245%; SGOT

151%; SGPT

646%), increased bilirubin and increased liver and kidney weights with associated pathological changes at 1000 ppm which were not severely adverse ( Refer to Table 3 for details).

For females at 1000 ppm, there was a decrease in the terminal body weight ( 8.9%). However, the findings were confounded by apparently fairly large standard deviations. With the exception of decreased terminal body weight, there were no significant differences from controls in body weight measurements. Significant increases in liver and kidney weights were seen only at week 26 and 78 ( kidney only). While increases in liver weight and findings of liver pathology were reported for females at 1000 ppm, these effects were either less consistent or occurred less frequently than those observed in males at this level. Other findings ( anemia, increased serum enzymes and pathological change such as foci of cellular alteration) showing evidence of toxicity, which were generally confined to the high dose were not noted in females. However, there was a significant increase in the incidence of chronic nephropathy among high dose females. The Committee, therefore, concluded that the highest dose tested in female rats was adequate to assess the carcinogenic potential of oxadiazon. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 8 2. Combined Chronic Toxicity/ Carcinogenicity Study in ICR JCL Mice Reference Y. Shirasu ( 1987). Oxadiazon 23 Month Chronic Toxicity and Oncogenicity Study in Mice. Institute of Environmental Toxicology, Tokyo, Japan; Study No. Not listed; Report dated February 1987. ( Unpublished) MRID: 40993301 A. Experimental Design Oxadiazon ( 95.9%) was administered to 80 ICR JCL mice ( 80/ sex/ dose) in the diet at 0, 3, 10, 100 or 1000 ppm ( equivalent to 0, 0.315, 1.09, 10.6 or 113 mg/ kg/ day for males or 0, 0.278, 0.92, 9.3 or 99 mg/ kg/ day for females) for 98 99 weeks ( the study was scheduled to run for 104 weeks but due to deaths, it was terminated at 98 99 weeks). Groups of 9 10 mice/ sex/ group were sacrificed at weeks 52 were subjected to pathology analysis.

B. Discussion of Tumor Data The incidences of liver tumors in male and female mice are presented in Table 5 and 6, respectively. For male mice, statistically significant increasing trends ( p< 0.01) were observed for liver adenomas, carcinomas and combined adenomas/ carcinomas ( Table 5). There were also significant increases by pair wise comparisons of the 100 and 1000 ppm dose groups with the controls for liver adenomas, combined adenomas/ carcinomas ( both at p < 0.01) and carcinomas ( p < 0.05 and p< 0.01, respectively). No significant increases were noted at lower doses ( 3 or 10 ppm). For female mice, statistically significant increasing trends ( p< 0.01) were noted for liver adenomas, carcinomas and combined adenomas/ carcinomas ( Table 6). There were statistically significant increases by pair wise comparison of the 1000 ppm dose group with the controls for adenomas ( p< 0.01), carcinomas ( p < 0.05) and combined adenomas/ carcinomas ( p < 0.01). Historical control data were not provided by the performing laboratory.

Table 5. Oxadiazon  ICR JCL Mouse Study:

Male Liver Tumor Rates+ and Exact Trend Test and Fisher's Exact Test Results ( p values) ( Brunsman, 2001) Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 9 Dose ( ppm)

0 3 10 100 1000 Adenomas (%)

p = 2/ 69 ( 3)

0.000** 7/ 71 ( 10)

0.090 2/ 71 ( 3)

0.676 12/ 69 ( 17)

0.005** 16a/ 71 ( 23)

0.000**

Carcinomas (%)

p= 3/ 69 ( 4)

0.000** 1/ 71 ( 1)

0.299 4/ 71 ( 6)

0.516 11/ 69 ( 16)

0.023* 29b/ 71 ( 41)

0.000**

Combined (%)

p = 5/ 69 ( 7)

0.000** 8/ 71 ( 11)

0.300 6/ 71 ( 8)

0.520 23/ 69 ( 33)

0.000** 45/ 71 ( 63)

0.000** + Number of tumor bearing animals/ Number of animals examined, excluding those that died before week 46. a First adenoma observed at week 52 in an interim sacrifice animal, dose 1000 ppm. b First carcinoma observed at week 46, dose 1000 ppm.

Note: Significance of trend denoted at control.

Significance of pair wise comparison with control denoted at dose level.

If *, then p < 0.05. If **, then p < 0.01. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 10 Table 6. Oxadiazon  ICR JCL Mouse Study: Female Liver Tumor Rates+ and Exact Trend Test and Fisher's Exact Test Results ( p values) ( Brunsman, 2001)

Dose ( ppm)

0 3 10 100 1000 Adenomas (%)

p = 0/ 52 ( 0)

0.000** 0/ 53 ( 0)

1.000 1a/ 46 ( 2)

0.469 1a/ 48 ( 2)

0.480 8a/ 51 ( 16)

0.003**

Carcinomas (%)

p= 1/ 52 ( 2)

0.000** 0/ 53 ( 0)

0.495 0/ 46 ( 0)

0.531 1/ 48 ( 2)

0.732 7b/ 51 ( 14)

0.028*

Combined (%)

p = 1/ 53 ( 2)

0.000** 0/ 53 ( 0)

0.495 1/ 46 ( 2)

0.721 2/ 48 ( 4)

0.470 15/ 51 ( 29)

0.000** + Number of tumor bearing animals/ Number of animals examined, excluding those that died or were sacrificed before week 53. a First adenoma observed at week 99 in final sacrifice animal simultaneously in doses of 10, 100 and 1000 ppm. b First carcinoma observed at week 83, dose 1000 ppm.

Note: Interim sacrifice animals are not included in this analysis. There were no liver tumors in any interim sacrifice animals.

Significance of trend denoted at control.

Significance of pair wise comparison with control denoted at dose level.

If *, then p < 0.05. If **, then p < 0.01. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 11 In addition to liver tumors in females, a significant ( p< 0.05) increase by pair wise comparison of the 1000 ppm dose group with the controls was noted for malignant lymphoma ( Table 7); however, no dose response was evident. The Committee concluded that these tumors were not treatment related because there was no dose response, the tumor response was variable and these tumors were not seen in the male mice. In addition, these tumors were also not reported in the previously performed mouse carcinogenicity and rat chronic/ carcinogenicity studies with oxadiazon. The historical control data were not available for comparison.

Table 7. Oxadiazon  ICR JCL Mouse Study: Female Lymphoma Tumor Rates+ and Exact Trend Test and Fisher's Exact Test Results ( p values) ( Brunsman, 2001)

Dose ( ppm)

0 3 10 100 1000 Malignant Lymphoma (%)

p = 16/ 80 ( 20)

0.067 25/ 79 ( 32)

0.067 19/ 80 ( 24)

0.351 21a/ 80 ( 26)

0.227 27/ 80 ( 34)

0.037*

+ Number of tumor bearing animals/ Number of animals examined, excluding those that died before week 19. a First malignant lymphoma observed at week 19, dose 100 ppm. Significance of trend denoted at control. Significance of pair wise comparison with control denoted at dose level. If *, then p < 0.05. If **, then p < 0.01.

C. Non neoplastic Lesions:

In 1991, the Agency requested the Registrant to provide new pathology summary tables and indicate the exact number of each tissue that was examined ( HED Document No. 008949) because the exact number of tissues/ organs examined could not be verified by the Reviewers. No correspondence regarding this request has been presented to HED. However, the recent review of data by the HED statistician indicated that none of the animals were excluded from the analyses. Therefore, the Committee concluded that the integrity of the study or the interpretation of the results is not compromised by this data deficiency. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 12 The non neoplastic changes in the liver observed in male and female mice are listed in Table 8. At 1000 ppm, there was a significant increase in the incidence of centrilobular liver swelling ( p< 0.001  ) , diffuse liver swelling ( p< 0.001

and  ) , brown pigment disposition ( p< 0.001

and  ) , and bile duct proliferation ( p< 0.001

) . The incidence of diffuse liver swelling and brown pigment disposition was also significantly increased at 100 ppm ( p< 0.001) but only in the males. The formation of brown pigment in the liver and kidneys of male mice is consistent with the inhibition of porphyrin biosynthesis by oxadiazon.

Other treatment related findings included a significant increase in the incidence of auricular hardening or thrombus in the heart of high dose males ( p< 0.05) and a significant ( p< 0.001) increase in brown pigment disposition in the proximal tubules of high dose male kidneys.

Table 8. Non neoplastic Lesions in the Liver of ICR JCL Mice Fed Dietary Administrations of Oxadiazon for 98 98 Weeks Lesions of the Liver Malesa Group ( ppm) Femalesa Group ( ppm)

0 3 10 100 1000 0 3 10 100 1000 Centrilobular Hepatocellular Swelling 1 1 0 3 2 1 0 1 1 14***

Diffuse Hepatocellular Swelling 1 2 5 45*** 67*** 3 5 1 2 24***

Brown Pigmentation Disposition 4 3 5 47*** 59*** 0 1 0 3 35***

Extra medullary Hematopoiesis 1 2 6 1 0 13 10 7 6 4*

Diffuse Hepatocellular Necrosis 1 2 4 16*** 7* 0 0 0 0 0 Bile Duct Proliferation 0 0 0 1 15*** 0 0 0 0 0 a 80 animals/ sex were reportedly examined at each dose level. * Significantly different ( p< 0.05) than the vehicle control by Fisher's Exact Test. ** Significantly different ( p< 0.01) than the vehicle control by Fisher's Exact Test. *** Significantly different ( p< 0.001) than the vehicle control by Fisher's Exact Test. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 13 D. Adequacy of Dosing for Assessment of Carcinogenic Potential Statistical evaluation of mortality indicated no significant incremental changes with increasing doses of oxadiazon in the male and female rats ( Brunsman, 2001). The CARC considered the dosing to be adequate and not excessive in males and females based on anemia and pathological changes in the liver at the highest dose tested ( HDT) which were not severely adverse ( Refer to Table 8 for details). The treatment related effects observed at 1000 ppm ( HDT) included transient anemia ( evident at week 52) in males and females, increased serum enzymes ( SGPT (

275 300%) , SGOT (

117%), ALP (

325%) and BUN (

44%) (

and  ) and at 100 ppm: increased SGPT (

147%) (

) ), increased liver weights ( absolute and relative) in males at week 52 and 98 and in females at week 98 and increased absolute and relative adrenal (

 week 98) and kidney (   week 98) weights.

IV. OTHER TOXICOLOGY DATA A. Mutagenicity and Cell Transformation Overall, the data indicate that oxadiazon is not mutagenic but does cause neoplastic cell transformation in vitro in Syrian hamster kidney BHK21 C13/ HRC1 cells. Nine acceptable mutagenicity studies were available for review. These studies satisfy the pre 1991 FIFRA guideline requirements . The summaries of these studies are presented below:

GENE MUTATION a) Salmonella typhimurium/ Escherichia coli reverse gene mutation assay. The assay was negative in S. typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100 and E. coli WP2 hcr up to the highest dose tested ( 2500  g/ plate  S9; 1000  g/ plate + S9) of 99.18% oxadiazon ( MRID No. 00069893).

b) S. typhimurium reverse gene mutation assay: The assay was negative in S. typhimurium strains TA1535, TA1537, TA1538, TA98 and TA100 exposed to 97.49% oxadiazon up to 5000  g/ plate+/ S9; cytotoxicity was seen at  3330  g/ plate  S9 ( MRID No. 41871701).

c) L5178Y TK +/ mouse lymphoma cell/ mammalian activation forward mutation assay: The assay was negative in cells treated with oxadiazon ( 95.5% a. i.) up to reproducibly cytotoxic levels in the absence of S9 activation ( 1000  g/ mL) and severely cytotoxic doses (  200  g/ mL) with S9 activation. Oxadiazon was insoluble at  62.5  g/ mL ( MRID No. 00115726). Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 14 d) L5178Y TK +/ mouse lymphoma cell/ mammalian activation forward mutation assay: The assay was negative in cells treated with recrystallized oxadiazon ( 100% a. i.) up to cytotoxic levels ( 1000  g/ mL  S9; 250  g/ mL + S9; MRID 00115729).

CHROMOSOME ABERRATIONS e) In vitro chromosome aberration assay in Chinese hamster ovary ( CHO) cells: The assay was negative in cells treated with oxadiazon ( 95.5% a. i.) up to cytotoxic concentrations ( 75  g/ mL  S9; 41.6  g/ mL + S9) and the limit of solubility (  416  g/ mL) ( MRID 00115730).

f) In vitro chromosome aberration assay in Chinese hamster ovary ( CHO) cells: The assay was negative in cells treated with recrystallized oxadiazon ( 100% a. i.) up to cytotoxic concentrations ( 200  g/ mL  S9; 500  g/ mL + S9) and the limit of solubility ( 667  g/ mL  S9; 200  g/ mL + S9; MRID 00115728).

OTHER MUTAGENIC MECHANISMS g) Unscheduled DNA Synthesis( UDS) in primary rat hepatocytes assay: The test was negative in hepatocytes exposed to oxadiazon ( 95.5% a. i.) to cytotoxic concentrations (  100 µ g/ mL) and the limit of solubility (  50 µ g/ mL) ( MRID No. 00115727).

h) UDS in primary rat hepatocytes assay: The test was negative in hepatocytes exposed to recrystallized oxadiazon ( 100% a. i.) up to cytotoxic concentrations ( 100 500 µ g/ mL) and the limit of solubility (  25 µ g/ mL) ( MRID No. 00115723).

CELL TRANSFORMATION i) In vitro cell transformation assay in Syrian hamster kidney BHK21 C13/ HRC1 cells: The test was positive both with and without S9 activation, based on the induction of transformation frequencies ( TFs)  5 times the solvent control value at the LD 50 . Oxadiazon ( 90% a. i.) and recrystallized oxadiazon ( 100 % a. i.) were tested up to cytotoxic concentrations with LD 50 values in the absence of S9 mix of 118 µ g/ mL and 200 µ g/ mL, respectively. In the presence of S9 mix, the LD 50 of oxadiazon was 69 µ g/ mL; however, the LD 50 for recrystallized oxadiazon was not determined as cell viability was 78% of the solvent control at the highest dose tested ( 400 µ g/ mL). The transformation frequencies ( the number of transformed colonies/ 106 surviving cells) at the LD 50 concentrations were 128 and 79 for cells treated with oxadiazon in the absence and presence of S9 mix, compared to the solvent control values of 4 and 5, respectively. Recrystallized oxadiazon induced transformation frequencies of 55 at the LD 50 in the absence of S9 mix and 60 at the highest dose tested in the presence of S9 mix. A positive dose response trend was generally apparent for both concentrations. This study is classified as acceptable ( nonguideline) ( MRID No. 00115703). Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 15 2. Conclusions Acceptable bacterial assays with  97.49% oxadiazon were negative for gene mutations in Salmonella typhimurium and Escherichia coli ( MRID Nos. 00069893 and 41871701). Similarly, neither 95.5% oxadiazon nor recrystallized Oxadiazon ( 100%) were mutagenic or clastogenic in cultured mammalian cells ( MRID Nos. 00115726, 00115729, 00115728 and 00115730) and did not cause UDS in primary rat hepatocytes ( MRID Nos. 00115727 and 00115723). There is, however, evidence that both formulations induced neoplastic transformation in Syrian hamster kidney cells both in the presence and in the absence of S9 activation ( MRID No. 00115703). The finding of positive cell transformation supports the evidence from mouse bioassays ( MRID Nos. 00444322, 00115733 and 40993301) and the rat long term studies ( MRID Nos. 00149003/ 00157780 and 40993401) of liver tumor induction.

B. Structural Activity Relationships The two structurally related compounds, azafenidin and sulfentrazone, are nonmutagenic and are not hepatocarcinogens in rats or mice.

Oxadiazon belongs to the class of oxadiazoles. While oxadiazon is only somewhat similar in structure to other pesticides that have a chlorinated phenol ring and a heterocyclic ring ( Figure 2), it shares some biological properties with azafenidin and sulfentrazone ( i. e., inhibition of protoporphyrinogen oxidase and/ or adverse effects on the hematopoietic system and the liver of rodents). Sulfentrazone produced equivocal results in the mouse lymphoma forward mutation assay, was not mutagenic in Salmonella and was neither clastogenic nor aneugenic in vivo. There was also no evidence of a carcinogenic effect in 2 year bioassays in rats and mice ( EPA, 1999). Azafenidin was not mutagenic in the available studies. The CARC agreed that the consensus classification for male rat thyroid tumors seen following administration of azafenidin should be in " Data are inadequate" category but no additional cancer studies were considered necessary nor would there be any quantification of human cancer risk.( CARC, 1999; HED Doc # 013794).

Figure 2. Structural Activity Relationships: Oxadiazon and Related Structures Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 16 N N O O Cl Cl O CH 3 CH 3 CH 3 C H 3 CH 3 N N O Cl Cl O N CH N N O Cl Cl O N CH Oxadiazon Azafenidin Sulfentrazone Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 17 N N O Cl Cl NH N CH 3 S O O CH 3 F F C. Mode of Action Studies The Mechanism of Toxicity Assessment Review Committee ( MTARC) determined that the available information does not support the proposed non genotoxic mode of action for oxadiazon induced liver tumors in rodents ( McCarroll, 2001).

The mechanistic studies including an unpublished study in Sprague Dawley rats ( MRID No. 42310001) and a published study by Richert et al., 1996 in Sprague Dawley rats, CD 1 mice and Beagle dogs were presented to the MTARC on February 8, 2001. The committee concluded that peroxisome proliferation may be a possible mode of action for oxadiazon induced liver tumors in rats and mice. However, there are deficiencies in the database which include lack of cell proliferation data in rat and mouse studies, lack of concordance between the dose response for peroxisomal enzymatic activity and liver tumor induction, and decrease rather than increase in catalase activity. Therefore, the available information is inadequate to determine the mode of action for oxadiazon induced liver tumors in rodents.

V. COMMITTEE'S ASSESSMENT OF THE WEIGHT OF THE EVIDENCE 1. Carcinogenicity The CARC concluded that: Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 18 ! In the combined chronic toxicity/ carcinogenicity study in Wistar rats, there was clear evidence that oxadiazon was carcinogenic to male rats because: 1) There were statistically significant ( p< 0.01) positive trends for liver adenomas, carcinomas and combined adenomas/ adenocarcinomas. There was also a statistically significant ( p< 0.05 or p< 0.01) increase by pair wise comparisons of the 100 and 1000 ppm ( 3.5 and 39 mg/ kg/ day, respectively) dose groups with the controls for liver adenomas ( 9% and 13% , respectively, vs 0% in controls) and combined adenomas/ carcinomas ( 9% and 23% vs 0% in controls) as well as liver carcinomas ( 10% vs 0% in controls) at 1000 ppm; and 2) The incidences of liver adenomas and carcinomas were outside the range for the published spontaneous rates ( range both for liver adenomas and carcinomas : 0% 2.5%). For females, there was a statistically significant increasing trend for liver carcinomas but there were no significant pair wise comparisons of liver tumors in treated females.

The highest dose level tested was considered to be adequate and not excessive for males based on decreased body weight gains as well as clinical and the clinical and histopatholgical liver changes observed which were not severely adverse. For female rats, the highest dose was considered to be adequate and not excessive based on an increased incidence of chronic nephropathy and liver changes. The survival of the animals was not affected by the treatment. The CARC concluded that the increases in both the benign and malignant liver tumors in the male rats were treatment related.

! In the combined chronic toxicity/ carcinogenicity study in ICR JCL mice, there was clear evidence that oxadiazon was carcinogenic to male and female mice because: 1) There were statistically significant ( p< 0.01) positive trends for liver adenomas, carcinomas and combined adenomas/ carcinomas in males and females. For males, there were also statistically significant ( p< 0.05 or p< 0.01) increases by pair wise comparisons of the 100 and 1000 ppm ( 10.6 and 113 mg/ kg/ day, respectively) dose groups with the controls for liver adenomas ( 17% and 23%, respectively, vs 3% in controls), carcinomas ( 33% and 63%, respectively, vs 4% in controls) and combined adenomas/ carcinomas ( 16% and 41% , respectively, vs 7% in controls). For females, there were also statistically significant ( p< 0.05 or < 0.01) increases by pair wise comparisons of the 1000 ppm dose group ( 99 mg/ kg/ day) with the controls for liver adenomas ( 16% vs 0% in controls), carcinomas ( 14% vs 2% in controls) and combined adenomas/ carcinomas ( 29% vs 2% in controls). The increase in the incidence of lymphomas in females was not considered to be treatment related because there was no doseresponse the tumor response was variable and this type of tumor was not seen in male mice or in earlier studies.

The highest dose level tested for the male and female mice was considered to be adequate and not excessive based on the findings of anemia and histopatholgical Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 19 changes in the liver which were not severely adverse. There were no adverse effects on the body weight gain and survival of the animals. The Committee concluded that the increases in both benign and malignant liver tumors in male and female mice were treatment related.

The positive results in an in vitro cell transformation assay are in concordance with the findings of liver tumor induction in the in vivo rodent studies.

2. Mutagenicity The CARC concluded that oxadiazon was negative for mutagenic potential in a battery of acceptable mutagenicity studies which satisfy the pre 1991 FIFRA guideline requirements. These studies included reverse gene mutation assays in bacteria, a mouse lymphoma forward gene mutation assay, chromosome aberration assays, and UDS assays. No new studies were requested by the CARC.

3. Structure Activity Relationships The structurally related compounds, azafenidin and sulfentrazone, are neither mutagenic nor liver carcinogens in rats or mice.

4. Mode of Action Studies The MTARC concluded that the available mechanistic data are insufficient to determine whether oxadiazon induced liver tumors in the rats and mice were associated with peroxisome proliferation. Nevertheless, the formation of brown pigment in the liver and kidneys of rats and mice is consistent with the inhibition of porphyrin biosynthesis by oxadiazon. It is caused by the disruption of the biosynthetic pathways producing heme that leads to accumulation of precursors throughout the body.

VI. CLASSIFICATION OF CARCINOGENIC POTENTIAL In accordance with the EPA Draft Guidelines for Carcinogen Risk Assessment ( July, 1999), the CARC classified oxadiazon into the category " Likely to be carcinogenic to humans" based on the following weight of the evidence considerations: Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 20 1. Treatment related benign and malignant liver tumors were observed in two species. There was clear evidence that oxadiazon induced both benign and malignant liver tumors in male Wistar rats and male and female ICR JCL mice. Liver tumors were also noted in earlier studies with F 344 rats and CD 1 mice using higher doses of oxadiazon that exceeded the MTD.

2. Oxadiazon was not mutagenic. However, it causes cell transformation in vitro; these results are in concordance with the carcinogenicity seen in in vivo rodent studies.

3. The available mechanistic studies do not support a non genotoxic mode of action for oxadiazon  induced liver tumors in rodents.

VII. QUANTIFICATION OF CARCINOGENIC POTENTIAL . For human cancer risk assessment, the CARC recommended using a linear low dose extrapolation approach based on the most potent liver tumors in the rats and mice. This approach is supported by the inadequacy of data on the mode of action for oxadiazon induced liver tumors in rodents. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 21 VII. BIBLIOGRAPHY MRID No. CITATION 40993401 Shirasu, Y. ( 1987). Oxadiazon  24 Month Chronic Toxicity and Carcinogenicity Study in Rats. Institute of Environmental Toxicology, Tokyo, Japan; Study No. Not listed; Report dated February 1987. ( Unpublished). HED Doc.# 08949.

40993301 Shirasu, Y. ( 1987). Oxadiazon 23 Month Chronic Toxicity and Carcinogenicity Study in Mice. Institute of Environmental Toxicology, Tokyo, Japan; Study No. Not listed; Report dated February 1987. ( Unpublished). HED Doc.# 08949.

 Brunsman, L. L. ( 2001). Oxadiazon Qualitative Risk Assessment ( Q 1 *) Based on SPF Wistar Rat and ICR_ JCL Mouse Dietary Studies. A memorandum from Lori L. Brunsman, Science Analyses Branch, Health Effects Division to Nancy McCarroll, Toxicology Branch, Health Effects Division, dated February 14, 2001. HED Doc # 014470.

 CARC. ( 1999). Evaluation of the carcinogenic potential of Azafenidin/ Cancer Assessment Document. Cancer Assessment Review Committee , Health Effects Division, Office of Pesticide Programs. Final Report dated October 18, 1999. HED Doc # 013794.

 EPA ( 1999). Office of Pesticide Programs List of Chemicals Evaluated for Carcinogenic Potential. Memorandum from William Burnam to Division Directors, Office of Pesticide Programs, Environmental Protection Agency. August 25, 1999.

 Farber, T. M.. ( 1987). Classification of Oncogenic Potential of Oxadiazon. Memorandum from Theodore M. Farber, Health Evaluation Division to Edwin F. Tinsworth, Registration Division, Office of Pesticide Programs, U. S. EPA., dated August 27, 1987. HED Doc # 007798.

 Litt, B. D. ( 1984). Carcinogenicity Risk Assessment for Oxadiazon. Memorandum from Bertram D. Litt, Toxicology Branch to Richard Mountfort Registration Division, Office of Pesticide Programs, U. S. EPA., dated November 21, 1984. HED Doc# 004097.

 Matringe, M., Camadro, J. M., Labbe, P., Scalla, R. ( 1989). Protoporphyrinogen oxidase inhibition by three peroxidizing herbicides: oxadiazon, LS 82 556 and M& B 39279. FEBS Letters 245, number 1, 2: 35 38. Oxadiazon ( 3 rd Review) Cancer Assessment Document Final Report 22  McCarroll, N. ( 2001). Oxadiazon: Assessment of Mode of Action on Liver Carcinogenicity. A memorandum from Nancy McCarroll, Toxicology Branch to William Burnham, Immediate Office, Office of Pesticide Programs, U. S. EPA., dated February 28, 2001.

 Quest, J. A. ( 1987). 2nd Peer Review of Oxadiazon. A memorandum from John A. Quest, Toxicology Branch to Richard Mountfort Registration Division, Office of Pesticide Programs, U. S. EPA., dated April 14, 1987. HED Doc # 07798  Richert, L., Price, S., Chesne, C., Maita, K. Carmichael, N. ( 1996). Comparison of the induction of hepatic peroxisome proliferation by the herbicide Oxadiazon in vivo in rats, mice, and dogs and in vitro in rat and human hepatocytes. Toxicol. Appl. Pharmacol 141: 35 43.

 Welsh, K. M. And Poteracki, J. ( 1994). Spontaneous neoplasms in control Wistar rats. Fundam Appl Toxicol 22: 65 72.


[Federal Register Volume 81, Number 63 (Friday, April 1, 2016)]
[Notices]
[Pages 18867-18868]
[FR Doc No: 2016-07396]

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DEPARTMENT OF HOMELAND SECURITY

Federal Emergency Management Agency

[Internal Agency Docket No. FEMA-4258-DR; Docket ID FEMA-2016-0001]

Oregon; Amendment No. 1 to Notice of a Major Disaster Declaration

AGENCY: Federal Emergency Management Agency, DHS.

ACTION: Notice.

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

SUMMARY: This notice amends the notice of a major disaster declaration
for the State of Oregon (FEMA-4258-DR), dated February 17, 2016, and
related determinations.

DATES: Effective Date: March 16, 2016.

FOR FURTHER INFORMATION CONTACT: Dean Webster, Office of Response and
Recovery, Federal Emergency Management Agency, 500 C Street SW.,
Washington, DC 20472,<PHONE_NUMBER>.

SUPPLEMENTARY INFORMATION: The notice of a major disaster declaration
for the State of Oregon is hereby amended to include the following area
among those areas determined to have been adversely affected by the
event declared a major disaster by the President in his declaration of
February 17, 2016.

    Douglas County for Public Assistance.
    The following Catalog of Federal Domestic Assistance Numbers
(CFDA) are to be used for reporting and drawing funds: 97.030,
Community Disaster Loans; 97.031, Cora Brown Fund; 97.032, Crisis
Counseling; 97.033, Disaster Legal Services; 97.034, Disaster
Unemployment Assistance (DUA); 97.046, Fire Management Assistance
Grant; 97.048, Disaster Housing Assistance to

Individuals and Households In Presidentially Declared Disaster
Areas; 97.049, Presidentially Declared Disaster Assistance--Disaster
Housing Operations for Individuals and Households; 97.050
Presidentially Declared Disaster Assistance to Individuals and
Households--Other Needs; 97.036, Disaster Grants--Public Assistance
(Presidentially Declared Disasters); 97.039, Hazard Mitigation
Grant.

W. Craig Fugate,
Administrator, Federal Emergency Management Agency.
[FR Doc. 2016-07396 Filed 3-31-16; 8:45 am]
 BILLING CODE 9111-23-P


[Federal Register Volume 79, Number 122 (Wednesday, June 25, 2014)]
[Rules and Regulations]
[Pages 36171-36176]
[FR Doc No: 2014-14948]

Vol. 79

Wednesday,

No. 122

June 25, 2014

Part III

Federal Communications Commission

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14 CFR Part 91

 Interpretation of the Special Rule for Model Aircraft; Final Rule

Federal Register / Vol. 79 , No. 122 / Wednesday, June 25, 2014 /
Rules and Regulations

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DEPARTMENT OF TRANSPORTATION

Federal Aviation Administration

14 CFR Part 91

[Docket No. FAA-2014-0396]

Interpretation of the Special Rule for Model Aircraft

AGENCY: Federal Aviation Administration (FAA), DOT.

ACTION: Notice of interpretation with request for comment.

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SUMMARY: This action provides interested persons with the opportunity
to comment on the FAA's interpretation of the special rule for model
aircraft established by Congress in the FAA Modernization and Reform
Act of 2012. In this interpretation, the FAA clarifies that: Model
aircraft must satisfy the criteria in the Act to qualify as model
aircraft and to be exempt from future FAA rulemaking action; and
consistent with the Act, if a model aircraft operator endangers the
safety of the National Airspace System, the FAA has the authority to
take enforcement action against those operators for those safety
violations.

DATES: Effective June 23, 2014. Comments must be received on or before
July 25, 2014.

ADDRESSES: You may send comments identified by docket number FAA-2014-
0396 using any of the following methods:
     Federal eRulemaking Portal: Go to http://www.regulations.gov and follow the online instructions for sending your
comments electronically.
     Mail: Send Comments to Docket Operations, M-30; US
Department of Transportation, 1200 New Jersey Avenue SE., West Building
Ground Floor, Room W12-140, West Building Ground Floor, Washington, DC
20590-0001.
     Hand Delivery: Take comments to Docket Operations in Room
W12-140 of the West Building Ground Floor at 1200 New Jersey Avenue
SE., Washington, DC, between 9 a.m. and 5 p.m., Monday through Friday,
except Federal holidays.
     Fax:<PHONE_NUMBER>.

FOR FURTHER INFORMATION CONTACT: Dean E. Griffith, Attorney,
Regulations Division, Office of the Chief Counsel, Federal Aviation
Administration, 800 Independence Avenue SW., Washington, DC 20591;
telephone:<PHONE_NUMBER>; email<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Comments Invited

    The FAA invites interested persons to submit written comments,
data, or views concerning this interpretation. The most helpful
comments reference a specific portion of the interpretation, explain
the reason for any recommended change, and include supporting data. To
ensure the docket does not contain duplicate comments, please send only
one copy of written comments, or if you are filing comments
electronically, please submit your comments only one time.
    The FAA will file in the docket all comments received, as well as a
report summarizing each substantive public contact with FAA personnel
concerning this interpretation. The FAA will consider all comments
received on or before the closing date for comments and any late-filed
comments if it is possible to do so without incurring expense or delay.
While this is the FAA's interpretation of statute and regulations
relevant to model aircraft, the FAA may modify this interpretation
based on comments received.

Availability of This Interpretation

    You can get an electronic copy using the Internet by--
    (1) Searching the Federal eRulemaking Portal (http://www.regulations.gov);
    (2) Visiting the FAA's Regulations and Policies Web page at http://www.faa.gov/regulations_policies/; or
    (3) Accessing the Government Printing Office's Web page at http://www.gpoaccess.gov/fr/index.html.

You can also get a copy by sending a request to the Federal Aviation
Administration, Office of Rulemaking, ARM-1, 800 Independence Avenue
SW., Washington, DC 20591, or by calling<PHONE_NUMBER>. Make sure to
identify the docket number or notice number of this proposal.

Background

    The FAA is issuing this interpretation because we have received
many inquiries regarding the scope of the special rule for model
aircraft in section 336 of the FAA Modernization and Reform Act of 2012
and the FAA's enforcement authority over model aircraft as affirmed by
the statute. In this interpretation, we explain the history of FAA
oversight of model aircraft operations and the new statutory
requirements that apply to model aircraft operations, and then clarify
how the FAA intends to apply its enforcement authority to model
aircraft operations that endanger the safety of the National Airspace
System (NAS).

Discussion of the Interpretation

I. Background of FAA Oversight of Model Aircraft Operations

    Historically, the FAA has considered model aircraft to be aircraft
that fall within the statutory and regulatory definitions of an
aircraft, as they are contrivances or devices that are ``invented,
used, or designed to navigate, or fly in, the air.'' See 49 U.S.C.
40102 and 14 CFR 1.1. As aircraft, these devices generally are subject
to FAA oversight and enforcement. However, consistent with FAA's
enforcement philosophy, FAA's oversight of model aircraft has been
guided by the risk that these operations present. The FAA first
recognized in 1981 that ``model aircraft can at times pose a hazard to
full-scale aircraft in flight and to persons and property on the
surface,'' and recommended a set of voluntary operating standards for
model aircraft operators to follow to mitigate these safety risks. See
Advisory Circular 91-57, Model Aircraft Operating Standards (June 9,
1981). These operating standards included restricting operations over
populated areas, limiting use of the devices around spectators until
after the devices had been flight tested and proven airworthy;
restricting operations to 400 feet above the surface; requiring that
the devices give right of way to, and avoid flying near manned
aircraft, and using observers to assist in operations.
    These guidelines were further clarified in 2007, when the FAA
issued a policy statement regarding unmanned aircraft systems (UAS)
operations in the NAS. See 72 FR 6689 (Feb. 13, 2007). In this policy
statement, the FAA also recognized that UAS fall within the statutory
and regulatory definition of ``aircraft'' as they are devices that are
``used or [are] intended to be used for flight in the air with no
onboard pilot.'' Id.; see also 49 U.S.C. 40102; 14 CFR 1.1. The FAA
noted that they can be ``as simple as a remotely controlled model
aircraft used for recreational purposes or as complex as surveillance
aircraft flying over hostile areas in warfare.'' The FAA then stated
its current policy regarding UAS based on the following three
categories: (1) UAS used as public aircraft; (2) UAS used as civil
aircraft; and (3) UAS used as model aircraft.
    With respect to UAS used as model aircraft, the FAA reiterated the
operating guidelines in AC 91-57, and further noted that to qualify as
a model aircraft, the aircraft would need to be operated purely for
recreational or hobby purposes, and within the visual line of sight of
the operator. The policy statement also clarified that AC 91-57

applied only to modelers and ``specifically excludes its use by persons
or companies for business purposes.'' 72 FR at 6690.

II. Requirements To Qualify as a Model Aircraft Under the FAA
Modernization and Reform Act of 2012 (Pub. L. 112-95, Section 336)

A. Statutory Requirements

    On February 14, 2012, the President signed into law the FAA
Modernization and Reform Act of 2012 (Pub. L. 112-95) (the Act), which
established, in Section 336, a ``special rule for model aircraft.'' In
Section 336, Congress confirmed the FAA's long-standing position that
model aircraft are aircraft. Under the terms of the Act, a model
aircraft is defined as ``an unmanned aircraft'' that is ``(1) capable
of sustained flight in the atmosphere; (2) flown within visual line of
sight of the person operating the aircraft; and (3) flown for hobby or
recreational purposes.'' Public Law 112-95, section 336(c). Congress'
intention to define model aircraft as aircraft is further established
by section 331(8) of the Act, which defines an unmanned aircraft as
``an aircraft that is operated without the possibility of direct human
intervention from within or on the aircraft.'' Congress' definition of
model aircraft is consistent with the FAA's existing definition of
aircraft as ``any contrivance invented, used, or designed to navigate,
or fly in, the air.'' 49 U.S.C. 40102; see also 14 CFR 1.1. Although
model aircraft may take many forms, at a base level model aircraft are
clearly ``invented, used, or designed'' to fly in the air. Id.
    Section 336 also prohibits the FAA from promulgating ``any rule or
regulation regarding a model aircraft, or an aircraft being developed
as a model aircraft'' if the following statutory requirements are met:
     The aircraft is flown strictly for hobby or recreational
use;
     the aircraft is operated in accordance with a community-
based set of safety guidelines and within the programming of a
nationwide community-based organization;
     the aircraft is limited to not more than 55 pounds unless
otherwise certified through a design, construction, inspection, flight
test, and operational safety program administered by a community-based
organization;
     the aircraft is operated in a manner that does not
interfere with and gives way to any manned aircraft; and
     when flown within 5 miles of an airport, the operator of
the aircraft provides the airport operator and the airport air traffic
control tower . . . with prior notice of the operation. . . .

Public Law 112-95, section 336(a)(1)-(5).
    Thus, based on the language of the statute, we conclude that
aircraft that meet the statutory definition and operational
requirements, as described above, would be exempt from future FAA
rulemaking action specifically regarding model aircraft. Model aircraft
that do not meet these statutory requirements are nonetheless unmanned
aircraft, and as such, are subject to all existing FAA regulations, as
well as future rulemaking action, and the FAA intends to apply its
regulations to such unmanned aircraft.

B. Model Aircraft Must Meet the Criteria in Section 336 To Be Exempt
From Future Rulemaking

    Congress directed that the FAA may not ``promulgate any rule or
regulation regarding a model aircraft, or an aircraft being developed
as a model aircraft'' if the aircraft is being operated, or being
developed to be operated, pursuant to the five criteria enumerated in
the statute as described above. Public Law 112-95, section 336(a). In
other words, Congress has restricted the FAA from promulgating
regulations, from the date when the statute was enacted, specifically
regarding model aircraft that meet the terms of the statute.
    However, the prohibition against future rulemaking is not a
complete bar on rulemaking that may have an effect on model aircraft.
As noted above, the rulemaking limitation applies only to rulemaking
actions specifically ``regarding a model aircraft or an aircraft being
developed as a model aircraft.'' Public Law 112-95, section 336(a).
Thus, the rulemaking prohibition would not apply in the case of general
rules that the FAA may issue or modify that apply to all aircraft, such
as rules addressing the use of airspace (e.g., the 2008 rule governing
VFR operations in the Washington, DC area) for safety or security
reasons. See 73 FR 46803. The statute does not require FAA to exempt
model aircraft from those rules because those rules are not
specifically regarding model aircraft. On the other hand, a model
aircraft operated pursuant to the terms of section 336 would
potentially be excepted from a UAS aircraft certification rule, for
example, because of the limitation on future rulemaking specifically
``regarding a model aircraft, or an aircraft being developed as a model
aircraft.'' Public Law 112-95, section 336(a). The FAA interprets the
section 336 rulemaking prohibition as one that must be evaluated on a
rule-by-rule basis.
    Although the FAA believes the statutory definition of a model
aircraft is clear, the FAA provides the following explanation of the
meanings of ``visual line of sight'' and ``hobby or recreational
purpose,'' terms used in the definition of model aircraft, because the
FAA has received a number of questions in this area.
    By definition, a model aircraft must be ``flown within visual line
of sight of the person operating the aircraft.'' Public Law 112-95,
section 336(c)(2).\1\ Based on the plain language of the statute, the
FAA interprets this requirement to mean that: (1) The aircraft must be
visible at all times to the operator; (2) that the operator must use
his or her own natural vision (which includes vision corrected by
standard eyeglasses or contact lenses) to observe the aircraft; and (3)
people other than the operator may not be used in lieu of the operator
for maintaining visual line of sight. Under the criteria above, visual
line of sight would mean that the operator has an unobstructed view of
the model aircraft. To ensure that the operator has the best view of
the aircraft, the statutory requirement would preclude the use of
vision-enhancing devices, such as binoculars, night vision goggles,
powered vision magnifying devices, and goggles designed to provide a
``first-person view'' from the model.\2\ Such devices would limit the
operator's field of view thereby reducing his or her ability to see-
and-avoid other aircraft in the area. Additionally, some of these
devices could dramatically increase the distance at which an operator
could see the aircraft, rendering the statutory visual-line-of-sight
requirements meaningless. Finally, based on the plain language of the
statute, which says that aircraft must be ``flown within the visual
line of sight of the person operating the aircraft,'' an operator could
not rely on another person to satisfy the visual line of sight
requirement. See id. (emphasis added). While the statute would not
preclude using an observer to augment the safety of the operation, the
operator must be able to view the aircraft at all times.
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    \1\ For purposes of the visual line of sight requirement,
``operator'' means the person manipulating the model aircraft's
controls.
    \2\ The FAA is aware that at least one community-based
organization permits ``first person view'' (FPV) operations during
which the hobbyist controls the aircraft while wearing goggles that
display images transmitted from a camera mounted in the front of the
model aircraft. While the intent of FPV is to provide a simulation
of what a pilot would see from the flight deck of a manned aircraft,
the goggles may obstruct an operator's vision, thereby preventing
the operator from keeping the model aircraft within his or her
visual line of sight at all times.

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    The statute requires model aircraft to be flown strictly for hobby
or recreational purposes. Because the statute and its legislative
history do not elaborate on the intended meaning of ``hobby or
recreational purposes,'' we look to their ordinary meaning and also the
FAA's previous interpretations to understand the direction provided by
Congress.\3\ A definition of ``hobby'' is a ``pursuit outside one's
regular occupation engaged in especially for relaxation.'' Merriam-
Webster Dictionary, available at www.merriam-webster.com (last accessed
June 9, 2014). A definition of recreation is ``refreshment of strength
and spirits after work; a means of refreshment or diversion.'' Id.
These uses are consistent with the FAA's 2007 policy on model aircraft
in which the Agency stated model aircraft operating guidelines did not
apply to ``persons or companies for business purposes.'' See 72 FR at
6690.\4\
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    \3\ In construing statutory language, agencies should assume
that the ordinary meaning of the language accurately expresses the
legislative purpose of Congress. Agencies are also permitted to
presume that Congress was aware of the agencies' administrative or
adjudicative interpretations of certain terms and intended to adopt
those meanings. See BedRoc Ltd. v. U.S., 541 U.S. 176, 183 (2004);
see also Haig v. Agee, 453 U.S. 280, 300 (1981); Lorillard v. Pons,
434 U.S. 575, 580-81 (1978).
    \4\ The FAA has also addressed recreational use of aircraft by
pilots in the Sport and Recreational Pilot Certificate rules, which
prohibit those pilots from acting as pilot in command of an airplane
carrying passengers or property for compensation or hire, or in
furtherance of a business. 14 CFR 61.101(e), 61.315(c). As discussed
in the Sport Pilot final rule, those prohibitions are designed to
limit those pilots to ``sport and recreational flying only.'' 69 FR
44772, 44839 (July 27, 2004).
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    Any operation not conducted strictly for hobby or recreation
purposes could not be operated under the special rule for model
aircraft. Clearly, commercial operations would not be hobby or
recreation flights.\5\ Likewise, flights that are in furtherance of a
business, or incidental to a person's business, would not be a hobby or
recreation flight. Flights conducted incidental to, and within the
scope of, a business where no common carriage is involved, generally
may operate under FAA's general operating rules of part 91. See Legal
Interpretation to Scott C. Burgess, from Rebecca B. MacPherson,
Assistant Chief Counsel for Regulations (Nov. 25, 2008). Although they
are not commercial operations conducted for compensation or hire, such
operations do not qualify as a hobby or recreation flight because of
the nexus between the operator's business and the operation of the
aircraft. See, e.g., Legal Interpretation to BSTC Corporation, from
Rebecca B. MacPherson, Assistant Chief Counsel for Regulations (June
22, 2009) (noting transportation of mining employees and guests appears
to be incidental to and within scope of operator's geological
business); Legal Interpretation to Scott C. Burgess (Nov. 25, 2008)
(noting transportation of automotive dealership employees and guests
must be incidental to and within scope of operator's real estate
development business).
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    \5\ A commercial operator is a ``person, who, for compensation
or hire, engages in the carriage by aircraft in air commerce of
persons or property. . . .'' See 14 CFR 1.1. The FAA would therefore
not consider a commercial operation to be ``flown strictly for hobby
or recreation purposes'' because it would be conducted for
compensation or hire.
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    To provide guidance, the following are examples of flights that
could be conducted as hobby or recreation flights and other types of
flights that would not be hobby or recreation.

------------------------------------------------------------------------
            Hobby or recreation                Not hobby or recreation
------------------------------------------------------------------------
Flying a model aircraft at the local model  Receiving money for
 aircraft club.                              demonstrating aerobatics
                                             with a model aircraft.
Taking photographs with a model aircraft    A realtor using a model
 for personal use.                           aircraft to photograph a
                                             property that he is trying
                                             to sell and using the
                                             photos in the property's
                                             real estate listing.
                                            A person photographing a
                                             property or event and
                                             selling the photos to
                                             someone else.
Using a model aircraft to move a box from   Delivering packages to
 point to point without any kind of          people for a fee.\6\
 compensation.
Viewing a field to determine whether crops  Determining whether crops
 need water when they are grown for          need to be watered that are
 personal enjoyment.                         grown as part of commercial
                                             farming operation.
------------------------------------------------------------------------

    Operations  that meet the section 336 definition of ``model
aircraft'' must also meet the five additional criteria for model
aircraft established in section 336(a) to be exempt from future
rulemaking regarding model aircraft. These criteria, with the exception
of the hobby and recreation standard that was previously addressed, are
explained below.
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    \6\ If an individual offers free shipping in association with a
purchase or other offer, FAA would construe the shipping to be in
furtherance of a business purpose, and thus, the operation would not
fall within the statutory requirement of recreation or hobby
purpose.
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    Section 336(a)(2) requires model aircraft to be operated within a
community-based set of safety guidelines and within the programming of
a nationwide community-based organization. Congress explained that it
intended ``nationwide community-based organization'' to mean, in part,
a ``membership based association that represents the aeromodeling
community within the Unites States; [and] provides its members a
comprehensive set of safety guidelines that underscores safe
aeromodeling operations within the National Airspace System and the
protection and safety of the general public on the ground. . . .'' U.S.
House, FAA Modernization and Reform Act of 2012, Conference Report (to
Accompany H.R. 658), 112 H. Rpt. 381 (Feb. 1, 2012) (discussion of
special rule for model aircraft). Based on this language, which
provides context to Congress' use of the term ``nationwide community-
based organization,'' the FAA expects that model aircraft operations
conducted under section 336(a) will be operated according to those
guidelines.\7\
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    \7\ ``[C]ommunity-based organizations,'' for example, would
include groups such as the Academy of Model Aeronautics and others
that meet the statutory definition.
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    Additionally, model aircraft are limited to 55 pounds or less. The
statutory language does not specify whether it applies to 55 pounds
unloaded or 55 pounds with other equipment, payload, or fuel, for
example, on the aircraft. The FAA believes that Congress intended for
the 55-pound limit to mean the weight of the aircraft at the time of
the operation. If the weight of the aircraft, alone, was the
determining factor then it could conceivably be loaded with equipment
or payload increasing the weight of the aircraft at time of takeoff
well in excess of 55 pounds, thereby increasing the risk of harm should
the operation not proceed as planned. The weight at the time of
operation is also consistent with the FAA's designation of small or
large aircraft which is determined by an aircraft's maximum
certificated takeoff weight. See, e.g., 14 CFR 1.1 (defining small and
large aircraft). Congress' recognition of the increased risk posed

by heavier aircraft is demonstrated by the more stringent requirements
for aircraft heavier than 55 pounds in the statute which are discussed
below. Accordingly, the FAA interprets this provision to mean the
weight of the aircraft at the time of the operation must not exceed 55
pounds, including the weight of any payload and fuel.
    The statute creates an exception for model aircraft that exceed the
55-pound weight limit if the aircraft is ``certified through a design,
construction, inspection, flight test, and operational safety program
administered by a community-based organization.'' Public Law 112-95,
section 336(a)(3). If a nationwide community-based organization has
provided its members with a set of safety guidelines that define a
design, construction, inspection, flight test, and operational safety
program then model aircraft constructed in accordance with that program
may exceed 55 pounds and operate in accordance with section 336(a).
    Model aircraft must not interfere with and must give way to any
manned aircraft. This requirement needs no further explanation, and the
FAA would expect that model aircraft operators abide by it.\8\ We note
that model aircraft interfering with, or that do not give way to,
manned aircraft would be subject to enforcement action under section
336(b), as further explained in section III below.
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    \8\ This requirement is consistent with longstanding FAA
guidance for model aircraft operators. See AC 91-57, para. 3
(advising model aircraft operators to ``[g]ive right of way to, and
avoid flying in the proximity of, full-scale aircraft.'').
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    Finally, the statute sets a requirement for model aircraft
operating within 5 miles \9\ of an airport to notify the airport
operator and control tower, where applicable, prior to
operating.10 11 If the model aircraft operator
provides notice of forthcoming operations which are then not authorized
by air traffic or objected to by the airport operator, the FAA expects
the model aircraft operator will not conduct the proposed flights. The
FAA would consider flying model aircraft over the objections of FAA air
traffic or airport operators to be endangering the safety of the NAS.
Additionally, we note that following this 5-mile notification procedure
would be read in conjunction with FAA rules governing airspace usage
discussed below.
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    \9\ For ease of determining distance, the FAA interprets the
statute to mean 5 statute miles.
    \10\ This requirement is consistent with longstanding FAA
guidance for model aircraft operators. See AC 91-57, para. 3
(advising model aircraft operators to notify an airport operator,
control tower, for flight service station when planning to operate
within three miles of an airport).
    \11\ If a group of modelers intends to operate in one area, one
person could contact air traffic control on behalf of the group.
Additionally, consistent with the statute, the FAA encourages
operators who fly from a permanent location within 5 miles of an
airport to ``establish a mutually-agreed upon operating procedure
with the airport operator and the airport air traffic control tower
(when an air traffic facility is located at the airport).''
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III. Scope of FAA's Enforcement Authority

    As discussed above, if a model aircraft is operated consistently
with the terms of section 336(a) and (c), then it would not be subject
to future FAA regulations regarding model aircraft. However, Congress
also recognized the potential for such operations to endanger other
aircraft and systems of the NAS. Therefore, it specifically stated that
``[n]othing in this section shall be construed to limit the authority
of the Administrator to pursue enforcement action against persons
operating model aircraft who endanger the safety of the national
airspace system.'' Public Law 112-95, section 336(b).
    Through this language, Congress specifically recognized the FAA's
existing authority to take enforcement action to protect the safety of
the NAS.\12\ Moreover, it did not limit the FAA's authority to take
enforcement action where a violation of a regulation results in the
endangerment of the NAS. As demonstrated by the FAA's statutory and
regulatory authorities, our charge to protect the safety of the NAS is
not only intended to protect users of the airspace, but is also
intended to protect persons and property on the ground.\13\
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    \12\ The NAS is broadly described as ``the common network of
U.S. airspace; air navigation facilities, equipment and services,
airports or landing areas; aeronautical charts, information and
services; rules, regulations and procedures, technical information,
and manpower and material. Included are system components shared
jointly with the military.'' See FAA Aeronautical Information Manual
(Apr. 3, 2014), available at http://www.faa.gov/air_traffic/publications/media/AIM_Basic_4-03-14.pdf.
    \13\ See 49 U.S.C. 40103(b)(2) (authorizing the FAA to prescribe
air traffic regulations to protect people and property on the
ground); Adm'r v. Johnson, NTSB Order No. EA-1008, 1977 WL 22279 at
*2 (May 10, 1977) (recognizing FAA authority to promulgate
regulations to protect persons and property on the ground); Adm'r v.
Page, NTSB Order No. EA-2786, 1988 WL 250725 at *3 (July 19, 1988)
(finding FAA's rulemaking and enforcement authority extends to areas
away from runways and taxiways--in this case the ramp of a fixed
base operator).
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    For example, the FAA regulates low-altitude operations to protect
people and property on the ground. The FAA permits aircraft operations
below 500 feet when flown over open water and in sparsely populated
areas. 14 CFR 91.119(c). Such operations may not be conducted ``closer
than 500 feet to any person, vessel, vehicle, or structure.'' Id.
Therefore, although such low-altitude operations may pose a lower risk
to aircraft flying much higher, the operation may still pose a risk to
persons and property on the ground warranting enforcement action when
conducted unsafely. See, e.g., Adm'r v. Kachalsky, NTSB Order No. EA-
4847, 2000 WL 1072332 (July 24, 2000) (affirming a violation of Sec.
91.119(c) for operating within 500 feet of a dwelling in a sparsely
populated area); Adm'r v. Beissel, NTSB Docket No. SE-19436, 2013 WL
7809754 (Dec. 11, 2014) (ordering suspension of a pilot certificate
when pilot flew a helicopter less than 40 feet above the surface of a
lake).
    Reading the broad reference to the NAS, along with Congress' clear
interest in ensuring that model aircraft are safely operated, we
conclude that Congress intended for the FAA to be able to rely on a
range of our existing regulations to protect users of the airspace and
people and property on the ground. Therefore, regardless of whether a
model aircraft satisfies the statutory definition and operational
requirements described above, if the model aircraft is operated in such
a manner that endangers the safety of the NAS, the FAA may take
enforcement action consistent with Congress' mandate.

IV. Examples of Regulations That Apply to Model Aircraft

    The FAA could apply several regulations in part 91 when determining
whether to take enforcement action against a model aircraft operator
for endangering the NAS. The FAA's general operating and flight rules
are housed in part 91 of the FAA's regulations. These rules are the
baseline rules that apply to all aircraft operated in the United States
with limited exceptions,\14\ and are the appropriate rules to apply
when evaluating model aircraft operations. See 14 CFR 91.1.
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    \14\ Part 91 does not apply to moored balloons, kites, unmanned
rockets, and unmanned free balloons, and ultralights vehicles
operated under 14 CFR parts 101 and 103.
---------------------------------------------------------------------------

    Rules relevant to these operations fall generally into three
categories: (1) How the aircraft is operated; (2) operating rules for
designated airspace; and, (3) special restrictions such as temporary
flight restrictions (TFRs) and notices to airmen (NOTAMs). These rules
are discussed in greater detail below.
    Rules addressing operation of the aircraft may include prohibitions
on careless or reckless operation and dropping objects so as to create
a hazard

to persons or property. See 14 CFR 91.13 through 91.15. Additionally,
Sec.  91.113 establishes right-of-way rules for converging
aircraft.\15\ Model aircraft that do not comply with those rules could
be subject to FAA enforcement action.
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    \15\ Additionally, model aircraft must not interfere with and
must always give way to any manned aircraft. Section 336(a)(4).
---------------------------------------------------------------------------

    Rules governing operations in designated airspace are found in
Sec. Sec.  91.126 through 91.135. In general, those rules establish
requirements for operating in the various classes of airspace, and near
airports in non-designated airspace to minimize risk of collision in
higher traffic airspace. Generally, if an operator is unable to comply
with the regulatory requirements for operating in a particular class of
airspace, the operator would need authorization from air traffic
control to operate in that area. See, e.g., 14 CFR 91.127(a),
91.129(a). Operations within restricted areas designated in part 73
would be prohibited without permission from the using or controlling
agency. Accordingly, as part of the requirements for model aircraft
operations within 5 miles of an airport set forth in section 336(a)(4)
of Public Law 112-95, the FAA would expect modelers operating model
aircraft in airspace covered by Sec. Sec.  91.126 through 91.135 and
part 73 to obtain authorization from air traffic control prior to
operating.
    The third category of rules relevant to model aircraft operations
are rules relating to operations in areas covered by temporary flight
restrictions and NOTAMs found in Sec. Sec.  91.137 through 91.145. The
FAA would expect that model aircraft operations comply with
restrictions on airspace when established under these rules.
    Other rules in part 91, or other parts of the regulations, may
apply to model aircraft operations, depending on the particular
circumstances of the operation. The regulations cited above are not
intended to be an exhaustive list of rules that could apply to model
aircraft operations. The FAA anticipates that the cited regulations are
the ones that would most commonly apply to model aircraft operations.

    Issued in Washington, DC, on June 18, 2014.
Michael P. Huerta,
Administrator.
[FR Doc. 2014-14948 Filed 6-23-14; 4:15 pm]
BILLING CODE 4910-13-P