Degree of Concern Analysis and Residual Uncertainties Since there is evidence of increased susceptibility of the young following exposure to Atrazine in the rabbit developmental study and in several special studies conducted to evaluate endocrine effects, HIARC performed a Degree of Concern Analysis to: 1) determine the level of concern for the effects observed when considered in the context of all available toxicity data; and 2) identify any residual concerns after establishing toxicity endpoints and traditional uncertainty factors to be used in the risk assessment of this chemical. If residual concerns are identified, HIARC examines whether these residual concerns can be addressed by a special FQPA safety factor and, if so, the size of the factor needed. The results of the HIARC Degree of Concern analyses for Atrazine ( and DACT) follow.

Prenatal Developmental Study with Atrazine in Rabbits The HIARC concluded that there is low concern for the qualitative increased susceptibility ( increased fetal resorptions at a dose level that resulted in decreased body weight gain and clinical signs in the maternal animal) because: 1) the NOAELs in the study are well characterized; and 2.) the fetal effects seen occurred at a high dose level ( 75 mg/ kg/ day).

The HIARC also concluded that there are no residual concerns for these effects considering that the Acute RfD established for Atrazine/ DACT is based on a NOAEL of 10 mg/ kg which is protective of the fetal effects observed at 75 mg/ kg/ day in the developmental rabbit study."

It is fair to say that this distinction between quantitative and qualitative sensitivity could have been made clearer and captured more fully in the risk assessment. It is reasonable to say that all aspects of atrazine's toxicity have neither been fully studied nor understood. However, these residual uncertainties surrounding atrazine's toxic effects on development and reproductive consequences for the young were clearly considered and ultimately formed the basis for 52 maintaining the full 10X FQPA SF along with residual uncertainties regarding exposure.

The portions of the comment referring to the endocrine effects in frogs has not been fully explored at this time as those results were just emerging at the time of the atrazine public technical briefing. HED must defer to the Environmental Fate and Effects Division ( EFED) as to the validity of these emerging findings. EPA expects to convene a Scientific Advisory Panel in the Summer 2003 to discuss the frog issue.

Comment Pesticides in general, and atrazine in particular occur widely in surface and drinking water. The risk assessment fails to include an analysis of the aggregate risk posed by atrazine and its metabolites, as well as an analysis of multiple pesticides in drinking water. The human health risk assessment does not adequately consider exposures to atrazine through drinking water and air.

HED Response HED agrees with the case made by the NYSAGO that atrazine contamination in US surface waters is widespread as seen from the USGS' variety of databases on water quality. Atrazine is present in surface waters in the US typically at low levels between 0.1 and 1 ppb. However, the kinds of data collected by the USGS to determine the quality of US waters, i. e., raw water in streams, lakes, creeks, rivers, ditches is applicable to ecological risk assessments rather than risk assessments for human health. These data do not represent pesticide concentrations in raw water at intake points into drinking water facilities but may be miles upstream, and consequently do not reflect the influence of dilution, treatment, and distribution effects within the treatment facility that all may affect pesticide concentrations in finished drinking water. These data were used appropriately by OPP in the ecological risk assessment, but should not be used in human health assessments. OPP's human health risk assessments are necessarily health based, quantitative, and linked to a toxic endpoint for health effects rather than qualitative and based on general occurrence information.

OPP's human health risk assessment was based on finished drinking water from a variety of sources including compliance monitoring under the SDWA and more intensive monitoring programs of drinking water in CWS in areas with known high use of and exposures to atrazine. The data used reflect a database biased towards CWS with atrazine exposure. The exposure assessment considered each of ~ 4000 CWS using surface water with data on atrazine serving 55 million + people and representing ~ 40% of all CWS in the US using surface water, and is believed to reflect all CWS reporting data on atrazine. Data on 418 CWS using groundwater ( 50% of which were the CWS using groundwater with prior detections of atrazine reported under the SDWA) representing 14,115 CWSs serving 20.5 million people were assessed. In addition to 53 these data sets, 2 programs of intensive monitoring in CWS using surface water were used to estimate 90 day average exposures. One program included ~ 100 CWS and the other ~ 175 CWS. These CWS are believed to contain CWS with exposures to atrazine and the chlorinated metabolites that represent high end exposures. Although incomplete, these data sets represent the most robust data set for a pesticide in finished drinking water. OPP intentionally conducted a drinking water assessment using targeted monitoring data CWS by CWS in the interest of identifying specific CWS at risk. Although it is unlikely that all CWS with high atrazine exposures were identified, this assessment is believed to highlight not the entire extent of exposure but the likely high end of exposures. The OW is currently assessing the extent of these high end exposures.

HED agrees that the metabolites are formed and exposures to them must be included in the risk assessments. However, HED disagrees with the statement that the risk assessment fails to include aggregate exposures to atrazine and its metabolites. The human health risk assessment for atrazine included estimates of exposures to atrazine, desethyl atrazine ( DEA), des isopropyl atrazine ( DIA), and diaminochlorotriazine ( DACT) in food and drinking water. These four compounds are considered to have a common mechanism of toxicity and believed to have equivalent toxicity to the parent compound. A separate assessment for the hydroxy metabolites was also included in the risk assessment Exposure to the hydroxy metabolites were not aggregated with the exposure to atrazine and the chlorinated metabolites, as the hydroxy compounds are not believed to share a common mechanism of toxicity with the chlorotriazine compounds.

Concern was expressed that the real exposure to humans in the diet cannot be ignored. The details of the dietary assessments for atrazine and the chlorinated metabolites, as well as, the hydroxy atrazine dietary assessment showing that dietary ( food) exposures to chlorotriazines and hydroxy metabolites are insignificant (< 1% of the a PAD and cPADs) can be found at the following URL: http:// www. epa. gov/ oppsrrd1/ reregistration/ atrazine/ antici_ residues. pdf.

The comment expresses concern that the risk assessment did not include atmospheric deposition contributions to exposure or multiple pesticide exposures in the risk assessment. Because HED used monitoring data for surface water, the contribution of atrazine to water supplies as deposited by atmospheric transport and rain is captured, i. e., is inherent in the database. There was no need to estimate this contribution from drift with computer models, etc. Any contribution to the dietary exposure from rainwater is also reflected in the monitoring data used to assess dietary exposures. For a further discussion of atrazine in rain water and fog and multiple pesticides see HED Response to Dr. John Wargo on these issues on pp. 48  49. As to the chemical mixtures issue, HED acknowledges that pesticides co occur, but OPP has no 54 statutory authority to regulate or methodology to assess risks associated with chemical mixtures not based on a common mechanism of toxicity. OPP will conduct a risk assessment in the future for triazines with a common mechanism of toxicity.

Comment The human health risk assessment improperly applies a 3 fold uncertainty factor under the FQPA for residential exposures. The use of a 3 fold safety factor for residential exposures is wholly unjustified given the uncertainties associated with exposure.

HED Response The following excerpt is from the FQPA SFC memorandum dated April 8, 2002.

" The FQPA Safety Factor Committee concluded that an additional Special FQPA safety factor of 3X is adequate for assessing residential exposures to Atrazine / DACT because the concerns for drinking water ( described above) would have little or no impact on the residential exposure scenarios. The concerns for the effect of the neuroendocrine mode of action on the development of the young remain and the Committee concluded that there are reliable data to address these concerns through use of an additional Special FQPA Safety Factor of 3X ( Refer to Section I. 3. B for the rationale that this factor would be adequate to account for these hazard based residual uncertainties)."

In considering residential exposures under FQPA, the SFC determined that although there are residual hazard based uncertainties for atrazine that apply to the young, residual concerns for exposure uncertainties would be adequately covered by the 3X SF for hazard based concerns because of the conservative assumptions used to estimate children's residential exposure. These assumptions are based on the OPP's Standard Operating Procedures for Residential Exposure ( revised 2001), and can be reviewed in HED's occupational residential exposure chapter for the reregistration eligibility decision.

The risk estimates for residential exposures are considered to be conservative. A variety of data were used to estimate exposures, some of it chemical specific for atrazine. Residential handler exposure and risk estimates were conducted using two sets of surrogate chemical data: the Occupational and Residential Exposure Task Force ( ORETF) study data and the Residential Standard Operating Procedures ( SOPs). Generally, the Residential SOP data ( default assumptions) are more conservative than ORETF data. Both data sets show wide variations in exposure depending on individual behaviors. Dermal postapplication exposures to atrazine were based on the higher average daily residues from the chemical specific turf transferable residues ( TTR) study data, but also used standard assumptions for transfer coefficients. Oral ingestion 55 scenarios for liquid formulations are based on standard assumptions and formulae ( Residential SOPs) which are designed to be screening level. Oral ingestion scenarios for hand to mouth exposures from granular formulations are based on a chemical specific study designed to determine the residue and/ or granules adhering to a wet hand after being repeatedly pressed onto turf treated with a granular formulation and are considered more refined. The risk estimates for children's residential exposures inclusive of a 3X hazard based FQPA SF are considered adequately protective.

Environment and Human Health, Inc. ( Dr. John Wargo):

Comment Dr. Wargo recommends that atrazine be cancelled based on the following points. The burden of proof should be shifted to the registrants to show the absence of hormonal effects especially in early life. Millions of Americans are routinely exposed to atrazine without their knowledge or consent. EPA has no capacity to continue registration while preventing human exposure. The Agency has not demonstrated that there is a reasonable certainty of no harm to children from atrazine exposure. EPA is only now beginning a cumulative assessment to include other triazines found to have a common mechanism of toxicity. Why should the public bear the burden of water testing and filtraiton? The registrant should.

HED Response The evidence that atrazine disrupts normal endocrine function is clear. Atrazine's documented neuroendocrine effects have become the main mechanism of toxicity, replacing the previous emphasis on carcinogenicity. Indeed, all of the toxic endpoints used in the atrazine human health risk assessment are based on this mechanism of toxicity. The registrant has devoted time and effort to researching the toxic mode of action in Sprague Dawley rats leading to early onset of mammary adenomas and carcinomas. It has been suggested that the registrant conduct special studies to assess the endocrine effects of atrazine on early life and development.

Dr. Wargo comments that contamination and exposure to atrazine is widespread. HED agrees that atrazine is commonly found in water in USGS surveys and is relatively ubiquitous in streams, creeks, rivers, and lakes located in atrazine use areas. However, OPP does not base risk assessments on the kinds of data routinely collected by the USGS because it is not indicative of human exposure through drinking water. Although filtration typically used by community water systems ( CWS) does not remove atrazine, raw water samples collected by USGS do not reflect treatment effects that do impact atrazine concentrations, i. e., activated carbon, nor do they reflect the effects of dilution and distribution systems at CWS. As mentioned, available drinking water monitoring data used in the risk assessment are limited, but are more reliable to estimate human 56 exposures than available ambient water quality monitoring data.

HED also agrees with the comment that people are routinely exposed to atrazine without their consent and knowledge. However, this can be said of pesticides in general as they are detected in foods that we eat as seen through the USDA's Pesticide Data Program ( PDP). In risk assessment, the key point is whether or not the levels of pesticides to which people are exposed result in hazardous impacts on their health. OPP's risk assessments are quantitative and are based on No Observed Adverse Effects Levels ( NOAELs) of toxic endpoints modified by uncertainty/ safety factors that are compared to estimates of exposures. OPP does not base its risk assessments on zero exposure as the comment seems to suggest it should.

HED's risk assessments for aggregate exposures of children to atrazine and its chlorinated degradates, as well as, hydroxy atrazine compounds indicate that although exposures through food are minimal ( insignificant), exposures via certain lawn use products and in specific CWS are above levels of concern. That is, in general, OPP could not demonstrate reasonable certainty of no harm for certain lawn uses of atrazine products. However, the converse is suggested for drinking water exposures, i. e., in general OPP could demonstrate reasonable certainty of no harm for drinking water exposures except in specific CWS. Although the rigor of this finding is subject to limitations and uncertainties in the database, these residual concerns about uncertainty in the exposure database were taken into account in applying the 10X FQPA safety factor to the drinking water assessments.

However, for those specific CWS undergoing or preparing to undergo intensive monitoring, residual uncertainties regarding the extent and magnitude of exposure to chlorotriazines have been removed, therefore supporting a reduction in the FQPA safety factor to 3X. Based on the availability of reliable drinking water exposure data, HED has recalculated the DWLOC ( drinking water level of concern) using a total risk assessment 300 fold uncertainty factor for those CWS currently undergoing or targeted for future intensive monitoring. For these CWS, the DWLOC for a 90 day average exposure becomes 37.5 ppb for total chlorotriazines. This value is based on an endpoint of 1.8 mg/ kg/ day, and a 300 fold uncertainty factor reflecting a 10 fold factor for interspecies variation, a 10 fold factor for intraspecies variability, and a 3 fold safety factor. The 3 fold safety factor reflects residual uncertainties associated with atrazine's toxic effects on the developing child only. For CWS without intensive monitoring as described above, the screening level DWLOC remains 12.5 ppb for total chlorotriazines.

In short, for those CWS with intensive monitoring, such that sufficient accuracy in the exposure assessments could be achieved, the portion of the FQPA safety factor reflecting residual uncertainties in the drinking water exposure database could be removed. Short of cancellation, 57 OPP does have options to mitigate these specific residential uses that are of concern for children, and to mitigate impacts of atrazine on drinking water in general via rate reductions, and on CWS in specific via rate reductions, and local restrictions on use followed up by intensive monitoring.

As noted, the cumulative assessment for the triazines has not been completed. Aggregate risk assessments for simazine and propazine are required first.

Comment Dr. Wargo brings up additional points regarding widespread atrazine contamination of water.

HED Response Regarding atrazine's use, OPP is aware of the large volume of atrazine use in the US and the resultant impact of atrazine on the nation's water supplies. OPP recognizes that part of any mitigation proposal should emphasize reducing this environmental loading. HED is also aware that countries in Europe have banned atrazine because of widespread occurrence at greater than 0.1 ppb. These bans are not based however on risk assessments but are related to policies in those countries.

Comment Dr. Wargo brings up additional points regarding atrazine's widespread contamination of water, averaging obscures peak concentrations, and degradates that are unregulated.

HED Response HED agrees that the current monitoring scheme under the SDWA obscures peaks of atrazine that may be occurring seasonally. To address this issue, HED has based its drinking water risk assessment on intermediate term exposures to 90 day average concentrations of atrazine and the chlorinated degradates rather than annual average concentrations. This assessment shows that seasonal peaks occur and are of greater concern for atrazine exposures than annual average exposures. HED defers to the Office of Water on the unregulated degradates comment.

Comment Dr. Wargo brings up additional points regarding exposures to atrazine is in fog and rainwater.

HED Response The comment expresses concern that the risk assessment did not include exposure to atrazine through fog and atmospheric deposition. Because HED used monitoring data for surface water to assess drinking water exposures, the contribution of atrazine to water supplies as deposited by atmospheric transport and rain is captured, i. e., is inherent in the database. There was no need to 3 Cooter, EJ, and WT Hutzell, USEPA, National Exposure Research Laboratory," A Regional Atmospheric Fate and Transport Model for Atrazine. 1. Development and Implementation", Environmental Science and Technology , Vol. 36, No. 19, 2002.

4 Cooter, EJ, and WT Hutzell, USEPA, National Exposure Research Laboratory," A Regional Atmospheric Fate and Transport Model for Atrazine. 1. Development and Implementation", Environmental Science and Technology , Vol. 36, No. 19, 2002.

58 estimate this contribution from drift with computer models, etc. Any contribution to the dietary exposure from rainwater is also reflected in the monitoring data used to assess dietary exposures. Based on the data available, dietary exposure estimates ranged up to 0.000017 mg/ kg/ day for food and up to 0.012 mg/ kg/ day for drinking water. The highest exposure estimates for food are approximately twice the maximum exposure estimate for air/ fog concentrations of atrazine, and drinking water exposures are at least 3 orders of magnitude higher than food or air/ fog exposures. Published literature indicates that atrazine has been detected and modeled in the atmosphere ( air/ fog) ranging from 10 9 up to 0.00001 mg/ kg/ day 3.

Although relative to drinking water and residential dermal exposures, exposures to atrazine through fog are expected to be minimal and not contribute significantly to risk, HED did consider inhalation of atrazine in its aggregate exposure assessments. These assessments consider inhalation exposure to the actual liquid and granular products containing atrazine as applied by the homeowner, which is expected to be in a much more concentrated form than atrazine dissolved in fog after being diffused and dissipated in the environment. HED estimates show that dermal exposures are greater than inhalation exposures for atrazine. Dermal exposures from use of atrazine products in and around the home are estimated to be 1.6 to 0.0034 mg/ kg/ day. Inhalation exposures for atrazine are estimated to be 0.00089 to 0.00001 mg/ kg/ day ( 1 to 5 orders of magnitude lower than dermal exposures). Published literature indicates that atrazine has been detected and modeled in the atmosphere ( air/ fog) ranging from 10 9 up to 0.00001 mg/ kg/ day 4. The maximum exposure estimate is for locations within 200 km of the point of application. These estimated exposures are 5 to 9 orders of magnitude lower than the maximum estimated dermal exposures and at most equal to the lowest estimated inhalation exposures for homeowners handling concentrated liquid or granular atrazine products as well as several orders of magnitude less than drinking water exposures.

Therefore, HED expects inhalation exposure through fog to be insignificant relative to drinking water, dermal and inhalation exposures from handling liquid atrazine products, which have been included in the risk assessment. Given the conservative assumptions resulting in high end estimates for the dermal and inhalation exposures used in the aggregate risk assessments, and the belief that exposure to atrazine through fog will be insignificant in comparison, HED believes any 59 potential exposures through fog have been adequately covered. Finally, HED believes that the 1000 fold uncertainty factor used for dietary exposure and the 300 fold uncertainty factor used for residential exposure used in conjunction with the conservative assumptions regarding residential exposure used in the atrazine human health risk assessment is adequately protective of aggregate exposures to atrazine.

Comment Dr. Wargo brings up additional points regarding atrazine in breast milk and fetal exposure.

HED Response Dr. Wargo expresses concern that atrazine may be transferred through breast milk and that this has not been considered in the risk assessment. However, HED points out that the human health risk assessment did consider both exposure and toxic effects associated with 1) the transfer of atrazine residues through milk via lactation, and 2) fetal exposures. The acute dietary risk assessment for food and drinking water is based on several developmental effects in offsrping and fetuses. One of these studies focused on the effects of exposure of the mother to atrazine on her suckling pups through lactation. This study showed prostatitis effects in the male pups exposed to atrazine through the mother's milk. The acute PAD is 0.01 mg/ kg/ day. This endpoint in conjunction with other developmental endpoints relevant to fetal effects formed the basis of the acute reference dose. The acute reference dose was determined through a weight of the evidence analysis of three developmental studies and this fourth study on exposure through lactation. HED's intermediate term and chronic risk assessments are based on an endpoint more than 5 times lower than the acute PAD or 0.0018 mg/ kg/ day. HED did not attempt to measure human breast milk for atrazine, but used instead used available information from animal feeding studies to estimate exposure. Since animals receive more atrazine in their diets than humans, this estimate of exposure through animal milk included in the dietary assessments should be conservative and protective of this type of exposure. HED therefore contends that not only exposure to atrazine through breast milk has been considered, but that relevant toxic endpoints regarding offspring and fetal effects have also been included in the human health risk assessments.

Comment Dr. Wargo brings up additional points regarding the inadequacy of filtration to remove atrazine from drinking water, and environmental justice issues.

HED Response Dr. Wargo states that conventional water treatment does not remove atrazine, but that atrazine must be removed by powdered activated carbon ( PAC). This means the wealthier communities 60 will treat while poor ones will not. HED agrees that conventional treatment will not remove atrazine and that PAC is required. As to the issue relating to the benefits of PAC only going to wealthier communities, HED must defer to the Office of Environmental Justice ( OEJ).

Comment Dr. Wargo expresses concern that the PLEX database is registrant generated and that the data are limited because too few samples are taken per year for a given community water system. This database will underestimate high seasonal exposures.

HED Response HED agrees that there are limitations in the database used to estimate drinking water exposures. However, although the data in the PLEX database were complied by the registrant, these data were not generated by the registrant as the comment states. These data are in fact generated under the SDWA; they are compliance monitoring data. The registrant organized, collected, and compiled these data by going to the individual CWS operators. HED agrees that some CWS with monitoring data under the SDWA may have been missed out of PLEX contributing to uncertainties in the exposure database. HED agrees that sampling under the SDWA is too infrequent to capture short term peaks, like seasonal pulses, of atrazine. Because of just these residual the uncertainties regarding the drinking water exposure database, along with residual uncertainties regarding developmental toxicity, HED determined that the full 10X FQPA safety factor should be applied to dietary risk assessments. As to increasing the frequency of compliance monitoring under the SDWA, HED must defer to OW on this issue.

Comment Dr. Wargo brings up additional points regarding health effects at high doses including mammary tumors resulting from lifetime exposures.

HED Response HED agrees that atrazine at high doses has been associated with a variety of health consequences in test animals, some but not all being relevant to humans. HED believes that the most important/ dominant health consequences known to date have been reflected in the human health risk assessment.

Comment Dr. Wargo states that the risk assessment document concludes that the atrazine toxicity database is complete, in spite of a lack of acute, sub chronic, and DNT studies. 61 HED Response The HIARC document dated April 5, 2002 states that the toxicity database for atrazine is complete and adequate to evaluate potential adverse health consequences to infants and children under FQPA. Atrazine has one of the most extensive databases of any pesticide. The toxicity database is complete as per OPPTS Guideline requirements for atrazine. The DNT is not a guideline study, and the DNT is not appropriate to assess pituitary/ endocrine function effects. For this reason, a DNT study has not been required. Similarly, acute and sub chronic neurotoxicity studies were not required for atrazine because the kinds of effects these studies test for ( functional battery tests) are not expected for atrazine. Rather, the HIARC recommended special studies designed to examine atrazne's specific neuroendocrine mode of action as more useful.

Comment Dr. Wargo expresses concerns regarding atrazine's effects on growth and development, and its potential as a carcinogen. He cites previously reviewed epidemiology studies and a case study in Louisiana at an atrazine manufacturing plant as evidence for continued concern regarding atrazine's carcinogenic potential. He notes the many alarming hormonal effects of atrazine, particularly for children.

HED Response HED shares Dr. Wargo's concern for atrazine's effects on development and growth in the young. The risk assessment is based on toxic endpoints that are all related to either developmental or reproductive effects in keeping with atrazine's main mode of toxic action, i. e, neuroendocrine effects. Based on this concern, HED's HIARC and FQPA committees determined that a 10X safety factor for children was warranted based in part on residual uncertainties regarding atrazine's effects on growth and development along with uncertainties in the exposure database. On this point the HIARC concluded...

" Since the focus of the testing with Atrazine in the young rat has been limited to short periods of dosing to specific developmental periods, uncertainties are raised for susceptibility during earlier developmental periods as well as for consequences of earlier developmental exposure with longer duration of dosing throughout development. The effects of neurotransmitters/ peptides ( known to be critical for normal development and which could potentially translate into severe effects in children that may not be manifested until later in life) have not been fully characterized. And as the FIFRA Scientific Advisory Panel noted, there are concerns for behavioral effects in the young resulting from Atrazine's CNS mode of action and the dose level at which these effects might occur 5SAP Report No. 2000 05; Atrazine: Hazard and Dose Response Assessment and Characterization. " Because of the rapid developmental brain changes... the influence of Atrazine on neurotransmitters in the hypothalamus and on GnRH may well have a differential, permanent effect on children. This phenomenon is the basis of the relatively new field of behavioral teratology. Atrazine could influence the migration of cells and the connectivity of the CNS. The influence of Atrazine on the hypothalamus and on GnRH may have a differential effect on children. This effect could be latent, and emerge later during the challenge of puberty, or during senescence. Behavioral alterations may be the most sensitive outcome. This possibility should be addressed...."

62 compared to reproductive/ developmental effects5."

Therefore, HED believes its risk assessment, which incorporates this safety factor, is protective of children.

Epidemiological evidence linking atrazine to cancer does not show a direct causal effect. HED cannot quantitate a cancer risk in the absence of a toxic endpoint linking atrazine exposure directly to cancer. Since mammary tumors in the Sprague Dawley rat have been the only tumors identified in association with atrazine exposure in test animals, and the toxic mechanism leading to these mammary tumors has been determined not to be operative in humans, HED has no toxic endpoint upon which to base a cancer assessment. However, the National Cancer Institute ( NCI) is currently conducting a study on cancer and pesticide exposures among the agricultural community of which atrazine is a part. These data and additional information on the incidence of prostate cancer at a Louisiana atrazine production facility were requested and reviewed. This review indicates that it appears that most of the increase in prostate cancer incidence at the St. Gabriel plant is likely due to intensive prostate specific antigen ( PSA) screening of employees conducted as part of the company's " Wellness Program." The study was insufficiently large and has limitations that prevent ruling out atrazine as a potential contributor to the increase observed. On balance, however, a role for atrazine seems unlikely because prostate cancer was found primarily in active employees who received intensive PSA screening; there was no increase in advanced tumors or mortality; and proximity to atrazine manufacturing did not appear to be correlated with risk.

Atrazine has also been tied to inflammation of the prostate in laboratory animals and changes in testosterone levels at high doses. However, neither condition has been tied to the increased risk of prostate cancer and the Agency concludes the animal data do not provide biologically plausible evidence to support atrazine as a cause of prostate cancer.

Other cancers besides prostate were found to have an elevated, though not statistically significant, increase in risk at the St. Gabriel plant. Other studies have suggested an increased risk for ovarian, breast, and other cancers, including non Hodgkin's lymphoma. However, these 63 studies are at best preliminary and should not serve as a basis for implicating atrazine as a human carcinogen due to their methodological limitations. See the IRED for further discussion.

Comment Dr. Wargo brings up the triazine common mechanism decision and the chemical mixture issue as a potential problem for atrazine as USGS studies have found that it co occurs with other pesticides.

HED Response HED expects to begin work on the triazine cumulative risk assessment after completing work on the aggregate simazine and aggregate propazine risk assessments. Until these single chemical risk assessments are completed, HED cannot comment on the outcome of the cumulative risk assessment for the triazine common mechanism group. As to the chemical mixtures issue, HED acknowledges that pesticides co occur, but OPP has no statutory authority to regulate or methodology to assess risks associated with chemical mixtures not based on a common mechanism of toxicity.

Beyond Pesticides/ NCAMP:

Comment NCAMP expresses concern that atrazine is widespread in water supplies and is a powerful endocrine disruptor. It cites several examples of endocrine effects in wildlife and test animals. They express concern for mammary tumors in rats exposed to atrazine and cite epidemiological studies' results to bolster this concern including the prostate cancer study at the St. Gabriel facility. NCAMP also provides mitigation measures for atrazine including: strengthening and enforcing the drinking water standard, banning all residential uses, and switching to widely available alternatives.

HED Response HED agrees with NCAMP that atrazine is an endocrine disruptor. The human health risk assessment has been based entirely on developmental and reproductive effects believed to be driven by a neuroendocrine mode of action believed to common to atrazine, its chlorinated degradates, and simazine and propazine. However, HED must defer to the EFED for a response on the specific wildlife effects noted.

The mammary tumors in the female Sprague Dawley rat have been attributed to atrazine's ability to affect the neuroendocrine system in the rat. However, the actual mechanism by which tumor formation occurs was determined by a June 2000 SAP to be " unlikely to be operative in 64 humans". Although the tumor formation in the rat and consequently the cancer endpoint are no longer considered relevant to human health, atrazine's ability to alter hypothalamic/ pituitary function in test animals is considered to be relevant to humans, and consequently, the entire human health risk assessment was based on toxic endpoints reflecting a neuroendocrine mode of action.

As to the epidemiological evidence for cancer in humans, the available epidemiologic data on atrazine do not make a direct causal link between atrazine and cancer. See the response to Dr. Wargo on the cancer issue on p. 51 and the IRED for further discussion.

By way of history, OPP has reviewed the many epidemiological studies on atrazine cited by NCAMP. These studies deal with various cancers of the ovary, prostate, colon, breast, leukemia, non Hodgkin's lymphoma. The results of these reviews can be found in their entirety in the following memoranda: " Review of Atrazine Incident Reports", DP Barcode: D270014, " Review of five epidemiological published articles for SAP", DP Barcode: D262405, and " A Follow up Study of Mortality Among Workers at the Novartis St. Gabriel Plant & Follow up Study of Cancer Incidence Among Workers in Triazine Related Operations at the St. Gabriel Plant, DP Barcode: D281568 & D278933. The studies reviewed are: IARC Overall Evaluation of Carcinogenicity to Humans, " A Follow up Study of Workers at the Ciba Geigy St. Gabriel Plant", E. Delzell, et al, April 8, 1996, " Atrazine, An Epidemiological Study at the Schweizerhalle Plant", R. Gass et al., January 15, 1993, Ciba Geigy Herbicide Mortality Study, " Ovarian Mesothelial Tumors and Herbicides: A Case Control Study", Donna, et al., 1984, " Triazine Herbicides and Ovarian Epithelial Neoplasms, Donna, et al., 1989, " Agricultural Herbicide Use and Risk of Lymphoma and Soft Tissue Sarcoma", Hoar, et al., 1986, " Pesticide Exposures and Other Agricultural Risk Factors for Leukemia Among Men in Iowa and Minnesota", Brown, et al., 1990, " Herbicides and Colon Cancer, Hoar, et al., 1985, " A Case Control Study of Non Hodgkin's Lymphoma and Agricultural Factors in Eastern Nebraska, Zahm, et al., 1988, " Farming and Non Hodgkin's Lymphoma, Cantor, et al., 1985, " Role of the Herbicide Atrazine in the Development of Non Hodgkin's Lymphoma ", Zahm, et al., 1993, " Triazine Herbicide Exposure and Breast Cancer Incidence: An Ecological Study of Kentucky Counties", Kettles, et al., 1997, and " Correlation Analysis of Pesticide use Data and Cancer Incidence Rates in California Counties", Mills, et al., 1998.

In summary, reviews of the epidemiological studies dealing with prostate cancers and exposure to atrazine conclude that the increases in prostate cancers among workers manufacturing atrazine are attributable to the increased PSA screening conducted at the plants as a part of routine checkups at the plants, and could not be conclusively linked to atrazine exposure. The reviews of studies dealing with non Hodgkin's lymphoma ( NHL) concluded that there was little to no 65 increase in the risk of NHL attributable to the agricultural use of atrazine after adjustment for the use of other pesticides, specifically 2,4 D and organophosphates. Or put another way, there is little evidence that atrazine exposure explains any appreciable increase in NHL over the last 15 years in the US. Reviews of studies dealing with ovarian cancers conclude that definite exposure to triazines was associated with a 2 to 3 fold increase of borderline significance in the risk for ovarian cancer, but that confirmatory studies were needed as this study was small and potentially confounded by exposure to other herbicides, which was not controlled for in this study. Reviews of studies for leukemia conclude that the results for an association between leukemia and atrazine are unremarkable. Reviews of studies on breast cancers show only modest increases in risk that are in the same range as non chemical risk factors not measured. The reviews conclude that in general, epidemiological studies containing information on atrazine exposures and cancer either indicate no significant increases in cancer risk that is directly associated with atrazine exposure, or raise more questions than they answer.

OPP concludes that " the results of the human epidemiology studies do not provide clear evidence of an association between triazines and cancer. Some of the studies, particularly those in which hormone responsive cancers such as breast, ovary and prostate, were examined, are suggestive of a possible association. There is also suggestive evidence of a possible association of triazine exposure and NHL. Further epidemiologic research is needed  especially in the area of hormone responsive cancers" ( Final Report  Atrazine: Hazard and Dose Response Assessment and Characterization, Part B Hazard Assessment and Review of Available Studies, report prepared for June 2000 SAP or www. epa. gov/ scipoly/ sap/ 2000/ index. htm# June 27).

Regarding strengthening and enforcing the atrazine drinking water standard in general, HED must defer to the OW. However, HED recognizes that atrazine is widespread in the Midwest. The majority of community water systems ( CWS) with risk estimates exceeding levels of concern are located in the Midwest. As to the CWS identified in the OPP human health risk assessment, mitigation to reduce the impacts of atrazine on those CWS is currently being discussed and will be negotiated with the registrant as part of a reregistration eligibility decision. HED agrees that residential uses of atrazine show risk estimates of concern for children, particularly for children playing on lawns shortly after application of liquid products. Mitigation for those uses and exposure patterns will be discussed as a part of the reregistration eligibility decision.

HED must defer to the BEAD regarding the availability of atrazine alternatives. 66 People for the Ethical Treatment of Animals ( PETA):

Comment PETA, believing the current MCL for atrazine is based on the rat study in which mammary female tumors in Sprague Dawley rats were noted, states that the mode of action behind the formation of these tumors is " not relevant to humans because there are considerable differences between the hypothalmic pituitary ovarian functions in humans and rats". Given this finding, they question how EPA can go forward with animal testing under the endocrine disruptor screening program if it has been decided that these tests don't apply to humans.

HED Response PETA correctly notes that the tumors associated with the Sprague Dawley rat are based on a specific toxic mechanism " not likely to be operative in humans" ( June 2000 SAP report). However, the same SAP noted that although the mechanism resulting in mammary tumor formation in the Sprague Dawley rat is not relevant to humans, the potential for atrazine to alter the function of the hypothalamus/ pituitary in a generic neuroendocrine mode of action is. To complete the SAP's thoughts on the subject, the following is an excerpt from the human health risk assessment for atrazine,

" Atrazine alters hypothalamic gonadotrophin releasing hormone ( GnRH) release in rats.

There are also some data that indicate that atrazine diminishes norepinephrine in the rat hypothalamus as an initial or early site of action which in turn leads to diminished GnRH release. Atrazine also increases dopamine levels which can result in a diminished pituitary secretion of prolactin. Therefore, atrazine appears to operate at the level of the hypothalamus. In both humans and rats, hypothalamic GnRH controls pituitary hormone secretion ( e. g., luteinizing hormone ( LH), and prolactin ( PRL). The hypothalamicpituitary axis is involved in the development of the reproductive system, and its maintenance and functioning in adulthood. Additionally, reproductive hormones modulate the function of numerous other metabolic processes ( i. e., bone formation, and immune, central nervous system ( CNS) and cardiovascular functions). Therefore, altered hypothalamic pituitary function can potentially broadly affect an individual's functional status and lead to a variety of health consequences.

The report of the Scientific Advisory Panel ( SAP) convened in June 2000 to consider these health consequences of exposure to atrazine, indicated that ".. it is not unreasonable to expect that atrazine might cause adverse effects on hypothalamic pituitary function in humans." Therefore, atrazine's effect on ovarian cycling and the pre ovulatory LH surge ( as well as its effects on pregnancy, puberty, suckling induced PRL release which leads to 67 prostatitis) are viewed as neuroendocrinopathies or biomarkers indicative of atrazine's ability to alter hypothalamic pituitary function in general. It should be noted that atrazine's neuroendocrine effects have been demonstrated in several strains of rats ( SD, Long Evans, and Wistar)."

Therefore, PETA incorrectly interpreted the SAP report on atrazine in assuming that endocrine testing results will not be extrapolated to humans. In fact, the opposite is the case; the SAP viewed the endocrine effects in the rats as indicative of potential endocrine effects in humans. Consequently, the entire human health risk assessment for atrazine is based on developmental and reproductive endpoints seen in test animals believed to be associated with the neuroendocrine effects of atrazine.

As to the use of human dermal absorption data in the risk assessment, the revised risk assessment used a 6% dermal absorption factor based on human data. The revised preliminary risk assessment used the animal data modified by the human data.

California Department of Pesticide Regulation ( CDPR):

Comment California Department of Pesticide Regulation ( CDPR) comments that up regulation of aromatase may be the mechanism involved in sub chronic/ chronic effects seen in rat studies and used in the risk assessment. They cite endocrine effects in amphibian species in support of this hypothesis. They also state that sex organ effects are extremely sensitive to reduced food intake and as such, in the Wistar and SD rat, reduced organ weight, delayed preputial separation and delayed puberty cannot be considered direct effects of atrazine dosing. Their value for risk assessment must therefore be considered dubious. They cite a study involving exposure of male SD rats during postnatal days 22 47, in which the average body weight of the rats at 100 mg/ kg/ day was reduced by about 9%. The authors also pair fed a group and found that even mild food restriction resulted in reductions in serum testosterone concentration, weights of androgendependent organs, and serum LH concentration; the same deficits that were seen in atrazine rats. They concluded that the effects of atrazine on male reproductive tract in rats receiving greater than 50 mg/ kg/ day could not be distinguished from the effects of reduced food consumption. The dose levels in this study were 1, 2.5, 5, 10, 25, 50, 100, and 200 mg/ kg/ day.

HED Response Regarding aromatase, HED's response on page 17 is reiterated below.

The SAP was asked to comment on whether alternative modes of action ( re: mammary tumors) 68 have been sufficiently discussed and ruled out by the Agency. The SAP stated " There are no data that would suggest other plausible modes of action. The increased level of hormones and the increased level of hormones alone, can account for the increased incidence of mammary tumors in Sprague Dawley female rats. The proposed mode of action is plausible and each step in the pathway has been shown to be affected in atrazine treated rats. None of the effects are based on speculation.

Previously, OPP concluded that it is plausible that enhanced aromatase activity may have some influence on the development of mammary tumors in SD female rats. However, whether or not enhanced aromatase activity is a significant contribution to the carcinogenicity, or other effects, of atrazine remains to be determined. EPA acknowledged the fact that an increase in aromatase activity would be consistent with dose response increases in estradiol and estrone and decreases in testicular testosterone noted in a study that examined the effects of atrazine on pubertal development. The doses that resulted in effects on these hormones were well above doses that led to reproductive/ developmental effects. Additionally, it was acknowledged that it is plausible that enhanced aromatase activity may have some influence on the development of mammary tumors in SD female rats; however, there are no data to date on whether enhanced aromatase activity significantly contributes to the carcinogenicity observed. The effect of the chlorotriazines on aromatase remains an active research issue, in general.

The EPA's National Health and Environmental Research Laboratory ( Dr. Ralph Cooper's laboratory) have recently evaluated the effects of atrazine and DACT on aromatase activity in the rat. Preliminary results show that DACT does not effect aromatase activity and atrazine actually causes a decrease in aromatase, but only at high doses. Based on the weight of evidence, enhancing aromatase activity does not appear to be a mode of carcinogenic action, particularly given the recent findings of Ralph Cooper. Further, if this were a primary mode of action, a more consistent finding of tumors at estrogen sensitive sites would be anticipated in the rodent carcinogenicity studies. Lastly, the June 2000 FIFRA Scientific Advisory Panel was specifically asked about OPP's assessment of other possible other modes of carcinogenic action, and the SAP agreed that there is an insufficient basis to link effects on aromatase to the mammary gland tumor response in female Sprague Dawley rats.

With regard to research data relating to the effects of atrazine on amphibians, EPA has not yet reached conclusions on these data, and therefore does not have any specific comment on these research efforts. EPA is planning to convene an independent scientific peer review [ the FIFRA Science Advisory Panel ( SAP)] of information related to potential effects of atrazine on amphibians sometime in mid 2003. 69 Although atrazine and food restriction produce many of the same effects, they may do so by different mechanisms. The study cited by DPR did not show any effects at dose levels that did not affect bodyweight; however, the study used in the short term risk assessment did show effects at dose levels not affecting body weight. In the cited study by DPR, restricted food consumption was observed at dose levels greater than 50 mg/ kg/ day, and the effects on testosterone concentration, weights of androgen dependent organs, and serum LH concentration were observed only at the high dose levels > 50 [ at 100 and 200 mg/ kg/ day]. There were no apparent effects on these parameters at dose levels where body weight effects were not observed, which supports DPR's concern.

However, in the Stoker study [ pubertal study in males used for short term risk assessment], delayed preputial separation was observed at 12.5 mg/ kg/ day and above, ventral prostate weight was decreased at 50 mg/ kg/ day or greater, but body weights were decreased mainly at the 200 mg/ kg/ day dose level and in the pair fed control group. In this latter study, the delay in preputial separation and decreased ventral prostate weight were observed in the absence of any effect on body weight. In the pubertal assay [ used for short term risk assessment], the NOAEL is 6.25; LOAEL is 12.5 mg/ kg/ day. Body weights on post natal day ( PND) 23 [ start of dosing] at 12.5 mg/ kg/ day were 96% of control and 98% of control on the day of preputial separation [ PPS]; 92% on PND 43 and 95% on PND 53. Dose levels tested in this study were 6.25, 12.5, 25, 50, 100, 150, 200, and a pair fed group. At 50 mg/ kg/ day, body weight was greater than control on PND 23 and at PPS; 98% of control at all other times. At 100 mg/ kg/ day, 99% at PPS and 90% on PND 43, etc. There were changes [ delays] in PPS in atrazine groups that did not affect body weight and more severe delays in the high dose group that did display decreased body weight. Ventral prostate weight was decreased compared to the vehicle control at 50 mg/ kg/ day and greater, as was the pair fed group ; also an effect at a dose level not affecting body weight.

One member on the June 2000 SAP for atrazine felt strongly that the appetite suppressant properties of atrazine are what induces the neuroendocrine alterations seen following atrazine exposure. The easiest way to examine appetite suppression is simply to look at food consumption, which Cooper et al. did in the pubertal assays. If atrazine is an appetite suppressant then, clearly, atrazine exposed animals will show decreased food consumption.

One thing that becomes evident from examining food consumption in the studies from the atrazine database is that if atrazine causes appetite suppression, it does so only at higher doses ( above 20 mg/ kg/ day) and even then the appetite suppression is, at worst, mild. Dr. Cooper did see some mild suppression at high doses but nothing at lower doses causing effects. Food consumption data illustrating this point from 6 studies ( the 28 and 6 month LH surge studies, three 2 year bioassays and one 1 year bioassay) and their references are shown below: 70 The greatest decrease in food consumption seen in this set of 6 studies was at the 29.44 mg/ kg/ day group of the 28 day study. In this group of this study there was a 21% decrease in food consumption during week one. Other than this dose, at this time point in this study, no decrease in food consumption was greater than 8% compared to controls.

28 day LH surge study; MRID 43934406; TXR 013996 Food consumption. Values shown are in grams.

Control 2.5 5.0 40 200 Week 1 0= 129 SD= 15.8 0= 128 SD= 15.1 0= 129 SD= 12.7 0= 124* SD= 13.2 0= 102* SD= 12.4 Week 5 0= 143 SD= 15.7 0= 140 SD= 19.2 0= 141 SD= 18 0= 141 SD= 15.3 0= 133* SD= 15.7 Weeks 1 5 0= 671 SD= 62.7 0= 667 SD= 66.6 0= 675 SD= 58.8 0= 667 SD= 59 0= 620* SD= 60.2 * p# 0.05 compared to control.

In this study there is little effect of atrazine on food consumption at 40 mg/ kg/ day where LH surge suppression was noted. Food consumption between control and 40 mg/ kg/ day at 5 weeks and for the entire study differ by less than 1.5%. At week one there is a statistically significant difference between the two groups, however the percent difference is still only 3.9%.

6 month LH surge study; MRID 44152102;

Food consumption. Values shown are in grams.

Week 1 Week 13 Week 25 Weeks 1 25 Control 0= 124 SD= 17.4 0= 138 SD= 14.4 0= 137 SD= 16 0= 3438 SD= 255.1 1.8 mg/ kg 0= 131* SD= 16.6 0= 141 SD= 14.8 0= 143 SD= 16.1 0= 3462 SD= 259.6 3.65 mg/ kg 0= 127 SD= 16.7 0= 131* SD= 15.6 0= 135 SD= 19 0= 3455 SD= 302.9 29.44 0= 114* 0= 127* 0= 135 0= 3309* 71 mg/ kg SD= 11.1 SD= 12 SD= 14.9 SD= 293.7 * p# 0.05 compared to control At week 13 food consumption is statistically significantly decreased compared to controls, but this decrease is only 5%. For the entire study food consumption is similar between control and 3.65 mg/ kg/ day and is, in fact, a tiny bit greater at 3.65 compared to control.

In both 28 day and 6 month LH surge LH surge and estrous cycles are altered at atrazine doses which affect food consumption little or not at all.

Thakur terminal sacrifice study with SD; MRID 42204401 Food consumption. Values shown are in grams.

Control 3.79 23.01 Weeks 1 24 0= 2610.9 SD= 196 0= 2637.5 SD= 240.8 0= 2544 ( 2.5%) SD= 181.9 Weeks 1 52 0= 3659.7 SD= 287.3 0= 3661.7 SD= 275.9 0= 3573.1 ( 2.4%) SD= 242.5 Weeks 1 104 0= 5725 SD= 398.6 0= 5632.6 SD= 355.5 0= 5662.1 ( 1.1%) SD= 335.5 * p# 0.05 compared to control.

Morseth 2 year study intact vs OVX; MRID 44544701 Food consumption. Values shown are in grams. Food consumption measured weekly from weeks 1 13 and every 4th week thereafter Control 1.5 3.1 4.2 24.4 Weeks 1 21 0= 2049 0= 1988 0= 2095 0= 2071 0= 1939 ( 5.4%)

Weeks 1 52 0= 3145 0= 3153 0= 3266 0= 3252 0= 3078 ( 2.1%)

Weeks 1 104 0= 4874 SD= 266.3 0= 5075 SD= 359.5 0= 5118 SD= 499.2 0= 5213 SD= 383.6 0= 4830 SD= 343.5 72 ( 1.0%)

The food consumption data from the pair of 2 year bioassays shown above shows little indication of an appetite suppressant effect. The food consumption is decreased most at doses above 20 mg/ kg/ day at the early timepoints. Even then the decrease is only 5% at most ( compared to controls). Early onset of mammary tumors, particularly carcinomas was evident in both these studies at 3.79 and 4.2 mg/ kg/ day  doses at which food consumption was similar to control values ( and in fact was slightly increased compared to controls).

Female daily mean food consumption from Mayhew ( MRID 00141874). Values shown are in grams.

Control 0.5 mg/ kg/ day 3.5 mg/ kg/ day 25 mg/ kg/ day 50 mg/ kg/ day Week 1 17.5 17.8 17.9 16.1** 14.4**

Week 26 19.7 19.3 19.6 19.1 18.4*

Week 52 20.7 20.5 20 20 19.8 Week 104 18.1 17.4 17.3 18.1 16.5 * p < 0.05 ** p < 0.01 One year study; MRID 43934402 Mean weekly food consumption. Values shown are in grams.

Week 1 Week 26 Week 50 Control 0= 16.34 0= 17.23 0= 19.42 0.8 0= 16.66 0= 17.3 0= 18.68 1.7 0= 16.25 0= 17.0 0= 19.18 2.8 0= 16.27 0= 16.89 0= 18.12 4.1 0= 16.71 0= 16.83 0= 19.52 23.9 0= 15.8 0= 17.04 0= 18.55 73 The data from these two studies again shows that decreased food consumption occurred at above 20 mg/ kg/ day and the decreases were most severe at the early timepoints.

In conclusion, one member of the SAP ( Dr. Phil Landfield) has advanced an hypothesis that atrazine's appetite suppressant properties are what induces the neuroendocrine alterations leading to mammary tumors. This hypothesis first assumes that atrazine actually has appetite suppressant properties, and second, assumes that these properties induce the neuroendocrine alterations.

However, there is not strong evidence that atrazine has any appetite suppressant properties at all. Food consumption is decreased if the doses are high enough ( above 20 mg/ kg/ day), but it is rarely decreased by more than 10%. Even then, the effect is seen only in the first few weeks of dosing. The atrazine database provides ample evidence of neuroendocrine alterations ( and tumor development) occurring at doses below 20 mg/ kg/ day.


[Federal Register Volume 76, Number 97 (Thursday, May 19, 2011)]
[Notices]
[Pages 28966-28967]
[FR Doc No: 2011-12303]

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

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. RM93-11-000]

Revisions to Oil Pipeline Regulations Pursuant to the Energy
Policy Act of 1992; Notice of Annual Change in the Producer Price Index
for Finished Goods

    The Commission's regulations include a methodology for oil
pipelines to change their rates through use of an index system that
establishes ceiling levels for such rates. The Commission bases the
index system, found at 18 CFR 342.3, on the annual change in the
Producer Price Index for Finished Goods (PPI-FG), plus two point six
five percent (PPI-FG+2.65). The Commission determined in an ``Order
Establishing Index For Oil Price Change Ceiling Levels'' issued
December 16, 2010, that PPI-FG+2.65 is the appropriate oil pricing
index factor for pipelines to use for the five-year period commencing
July 1, 2011.\1\
---------------------------------------------------------------------------

    \1\ 133 FERC ] 61,228 at P 1 (2010).
---------------------------------------------------------------------------

    The regulations provide that the Commission will publish annually,
an index figure reflecting the final change in the PPI-FG, after the
Bureau of Labor Statistics publishes the final PPI-FG in May of each
calendar year. The annual average PPI-FG index figures were 172.5 for
2009 and 179.8 for 2010.\2\ Thus, the percent change (expressed as a
decimal) in the annual average PPI-FG from 2009 to 2010, plus 2.65
percent, is positive 0.068819.\3\ Oil pipelines must multiply their
July 1, 2010, through June 30, 2011, index ceiling levels by positive
1.068819 \4\ to compute their index ceiling levels for July 1, 2011,

through June 30, 2012, in accordance with 18 CFR 342.3(d). For guidance
in calculating the ceiling levels for each 12 month period beginning
January 1, l995,\5\ see Explorer Pipeline Company, 71 FERC 61,416 at
n.6 (1995).
---------------------------------------------------------------------------

    \2\ Bureau of Labor Statistics (BLS) publishes the final figure
in mid-May of each year. This figure is publicly available from the
Division of Industrial Prices and Price Indexes of the BLS, at (202)
691-7705, and in print in August in Table 1 of the annual data
supplement to the BLS publication Producer Price Indexes via the
Internet at http://www.bls.gov/ppi/home.htm. To obtain the BLS data,
scroll down to ``PPI Databases'' and click on ``Top Picks'' of the
Commodity Data including stage-of-processing indexes (Producer Price
Index--PPI). At the next screen, under the heading ``Producer Price
Index/Commodity Data,'' select the first box, ``Finished goods--
WPUSOP3000,'' then scroll all the way to the bottom of this screen
and click on Retrieve data.
    \3\ [179.8-172.5]/172.5 = 0.042319 + .0265 = 0.068819.
    \4\ 1 + 0.068819 = 1.068819.
    \5\ For a listing of all prior multipliers issued by the
Commission, see the Commission's Web site, http://www.ferc.gov/industries/oil/gen-info/pipeline-index.asp.
---------------------------------------------------------------------------

    In addition to publishing the full text of this Notice in the
Federal Register, the Commission provides all interested persons an
opportunity to view and/or print this Notice via the Internet through
FERC's Home Page (http://www.ferc.gov) and in FERC's Public Reference
Room during normal business hours (8:30 a.m. to 5 p.m. Eastern time) at
888 First Street, NE., Room 2A, Washington, DC 20426. The full text of
this Notice is available on FERC's Home Page at the eLibrary link. To
access this document in eLibrary, type the docket number excluding the
last three digits of this document in the docket number field and
follow other directions on the search page.
    User assistance is available for eLibrary and other aspects of
FERC's Web site during normal business hours. For assistance, please
contact the Commission's Online Support at 1-866-208-3676 (toll free)
or<PHONE_NUMBER> (e-mail at FERCOnlineSupport@ferc.gov), or the Public
Reference Room at<PHONE_NUMBER>, TTY<PHONE_NUMBER>. E-Mail the Public
Reference Room at<EMAIL_ADDRESS>
    Dated: May 12, 2011.
Kimberly D. Bose,
Secretary.
[FR Doc. 2011-12303 Filed 5-18-11; 8:45 am]
BILLING CODE 6717-01-P


EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 1 EPA National Community Recognition Program Validation of Beta Application Thank you very much for contributing your expertise and time to assist the EPA in creating this national recognition program for communities who are creating smart growth initiatives that also specifically enhance the health and well being of older Americans.

The purpose of the beta testing process is to establish content validity of the project questions and gather feedback for question revision through rankings by content area experts in smart growth and active aging, local/ county/ state officials, and others representing potential applicants to the recognition program. We also want to assess the ease of completing the on line instrument.

Instructions:

Please read the introductory section containing the definitions of the smart growth and active aging/ physical activity programming of interest, and the descriptions of the process and program levels. Applicants will also be asked to acknowledge their review of accompanying documents regarding specific components of smart growth policy, and the participation of a local aging services official in completion of the recognition program application.

Read each statement beginning on page 3 for items 1A through 5D and rate each on a scale of 1  10 as to how well it reflects the content described in the process and program definitions provided below. YOU DO NOT HAVE TO COMPLETE THE INFORMATION ABOUT THE PROGRAM ITSELF, ONLY THE SECTION REGARDING HOW WELL THE ITEM ASSESSES THE CONTENT REGARDING SMART GROWTH ( SG) and/ or PHYSICAL ACTIVITY ( PA). WE WANT TO DETERMINE IF THE ITEM IS CLEAR AND UNDERSTANDABLE TO YOU. Questions for you to complete are in red and bold type. Regardless of your rating, we encourage you to suggest any revision that would clarify the content of the item.

Introduction Definitions:

* Smart Growth ( SG): Smart Growth is defined as community development that serves the environment, community, economy, and public health. The principles of smart growth include: 1) Mix land use; 2) Take advantage of compact building design; 3) Create a range of housing opportunities and choices; 4) Create walkable neighborhoods; 5) Foster distinctive, attractive neighborhoods with a sense of place; 6) Preserve open space, farmland, natural beauty, and critical resources; 7) Strengthen and direct development towards existing communities; 8) Provide a variety of transportation choices; 9) Make development decisions predictable, fair, and cost effective; 10) Encourage community stakeholders collaboration in development decisions.

To be completed by applicant:

I have reviewed the accompanying policy and activity components that are integral to the smart growth principles above, and understand that they should form the basis for our community's responses to the application items for the Smart Growth and Active. Aging National Recognition Program. EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 2 * Active Aging/ Physical Activity ( PA): includes planning and implementing a variety of widely accessible programs and/ or self directed opportunities for those 60+ and which emphasize activities that increase endurance, strength, flexibility, balance, and the principles of injury prevention. These types of activities include walking, biking, fitness trails and similar activities/ programs at various levels of intensity to fit the capacities of participants. * This section will include additional resource links * Community assessment or survey: can include formal needs assessment or community survey or discussion of community needs with service providers with smart growth or active aging/ physical activity programming or opportunities in the community. * This section will include additional resource links * Denotes information link to definitions, examples, weblinks, etc Description of process and program levels:

Process I: Awareness of and general commitment to basic smart growth principles and active aging/ physical activity programs and opportunities.

Process II: Awareness of smart growth and active aging/ physical activity principles, applications and implementation strategies formulated with attention to linking smart growth and active aging/ physical activity programs and opportunities in the community.

Process III: Well established processes combining smart growth and active aging with coherent framework and broad smart growth and aging network community participation Well conceived and funded strategic attention to smart growth principles and active aging programs and opportunities; ability to mentor or serve as model for other communities. Processes are scalable, sustainable, and sharable,

Program I: Actively engaged in formulating pilot programs and activities combining smart growth and active aging.

Program II: Established/ expanding programs combining smart growth and active aging; engagement of broader segments of the community in program activity; active promotion of the program on a community basis.

Program III: Ongoing/ expanding programs on a wide community basis that are effectively applying principles of smart growth and active aging; wide community involvement of multiple sectors within the community; program funding sources established; ability to mentor or serve as a model program for other communities. Programs are scalable, sustainable, and sharable. EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 3 BETA Items Level1 1 A: SG Process I: Our community has defined goals or a mission for advancing or applying * smart growth principles.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 8____ Suggestions for revision:

1 B: SG Process I: Our community has conducted a * community assessment, survey or other planning activity for applying * smart growth principles.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: _ 9_____ Suggestions for revision: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 4 1 C: PA Process I: Our community has defined goals or a mission for increasing older adult participation in * active aging/ physical activity.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 8____ Suggestions for revision:

1 D: PA: Process I: Our community has conducted a * community assessment or survey, or reviewed information/ data for increasing older adult participation in active aging/ physical activity.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 9____ Suggestions for revision:

Level 2 2 A: SG: Process II: Our community's strategic development plan includes aspects of feasibility, cost, impact, time frame and leadership for applying smart growth principles.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 5 Describe Activity:

> How well does this item assess the content for Process II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 8____ Suggestions for revision:

2 B: SG: Process II: Our community is actively engaged in formulating plans and strategies for specifically linking smart growth initiatives with programs, amenities or opportunities that include active aging/ physical activity for older adults

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 10____ Suggestions for revision:

2 C: PA: Process II: Our community has a broad based planning process that includes feasibility, cost, impact, time frame and leadership for creating/ promoting active aging/ physical activity for aging adults.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 6 > How well does this item assess the content for Process II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 7____ Suggestions for revision: This question focuses more on the broad based process of Process III than Process II 2 D: PA: Process II: Our community has established interagency committees, task forces, or other community partnerships with local aging organizations, service providers, and agencies as a means of coordinating activities and programs with smart growth and active aging/ physical activity components.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Process II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: ___ 7___ Suggestions for revision: Same as above Level 3 3 A: SG & PA: Process III: Our community's comprehensive planning integrates smart growth principles and promotes application of these to encompass active aging/ physical activity programs and opportunities for older adults.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 7 > How well does this item assess the content for Process III:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 7____ Suggestions for revision: Only one question for Process III; does not address whether initiatives are funded ( I see there are more questions later combining process and program)

3 B: SG: Program I: Our community has legislative, zoning, comprehensive plan initiatives and other policies in place or in consideration that include provision for both smart growth and active aging/ physical activity programs or opportunities for older adults.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Program I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: ____ 9__ Suggestions for revision:

3 C: PA: Program I: Our community has created pilot programs, or has existing programs for active aging/ physical activity for older adults which take advantage of the resources and environments created by local smart growth activities such as safe walking area, biking amenities, age sensitive exercise trails, safe parks, etc. * This section will include additional resource links

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 8 > How well does this item assess the content for Program I:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 10____ Suggestions for revision:

Level 4 4 A: SG: Program II: Our community is increasing its capacity through budget allocation, staff resources, infrastructure improvement, etc. for systematically expanding existing initiatives that combine smart growth principles and planning and active aging/ physical activity programs and opportunities.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Program II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: ___ 10___ Suggestions for revision:

4 B: SG: Program II: Our community is reaching out to local/ county/ state officials and departments, land developers, and community organizations to expand the integration of smart growth and active aging/ physical activity programs.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 9 > How well does this item assess the content for Program II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: _ 10_____ Suggestions for revision:

4 C: PA: Program II: Our community includes gathering evidence about and evaluating the effectiveness of and level of participation in our active aging/ physical activity programs and opportunities for older adults.

Not at all

Just starting

Partially complete

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Program II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: ___ 8___ Suggestions for revision: Addressses just active aging and not smart growth 4 D: PA: Program II: Our community has an initiative that includes promotion, advertising, recruitment, and widely available programs and opportunities to engage more older adults in active aging/ physical activity.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 10 > How well does this item assess the content for Program II:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 8____ Suggestions for revision: Does not address smart growth.

Level 5 5 A: SG: Program/ Process III: Our community has already implemented, or has the capacity to implement a model program combining smart growth principles with programs emphasizing active aging/ physical activity for older adults.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Program/ Process III:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 10____ Suggestions for revision:

5 B: SG: Program/ Process III: Our community has a well established smart growth initiative and active aging/ physical activity programs and opportunities and is planning to expand these to a wider segment of our population as well as the partnerships that will support these programs.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 11 > How well does this item assess the content for Program/ Process III:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 8____

Suggestions for revision: Are " a wider segment of the population" and " partnerships" two different segments of the population? It seems like expansion to partnerships is a different concept and should be addressed separately.

5 C: PA: Program/ Process III: Our community has an established coalition of service providers, advocacy organizations, businesses and governmental agencies who are cooperating to create more innovative and widely available programs that integrate smart growth principles and active aging/ physical activity programs and opportunities.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Describe Activity:

> How well does this item assess the content for Program/ Process III:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: __ 9____ Suggestions for revision:

5 D: PA: Program/ Process III:

Our community has an existing model program integrating active aging/ physical activity and smart growth for older adults and we can provide technical assistance and a contact person to share information with other communities.

Not at all

Just starting

Partially completed

Fully Completed

Ongoing Please describe your program/ initiative below or attach additional information: EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 12 Contact Person for program/ initiative described above: Name:_____________________________________________ Title:______________________________________________ Organization:_______________________________________ Address:___________________________________________ ____________________________________________ City:________________________________ State:_____ Zip:__________ Phone:___________________ Fax:_________________ Email:__________________________________________

> How well does this item assess the content for Program/ Process III:

1 2 3 4 5 6 7 8 9 10 Not at all Adequately Very Well Your Score: _ 10_____ Suggestions for revision:

BETA TEST RESPONDENTS: PLEASE COMPLETE THE QUESTIONS BELOW:

> How was the process of completing this document for you and/ or your staff?

1 2 3 4 5 X6 7 8 9 10 Easy Somewhat Difficult Difficult If you rated this process with a score of 6   10, please suggest how we might make this questionnaire easier to complete: The difficulty was in keeping the six different processes and programs clear and straight in one's mind in order to evaluate whether the question addressed the relevant concept.

> Approximately how long did it take to complete this? __ 1___ hrs. _____ min. EPA Smart Growth & Active Aging National Recognition Program DCTM_ ARP. doc 13 > Would you recommend applying for this recognition program to other communities? ___ Yes _ X__ No Applicant completing this beta test form:

Name: __ Karin Franklin ______________________________________

Title: ___ Director___________________________________________

Organization: Dept. of Planning & Community Development____________________________ Address: 410 E. Washington St.________________________________________ ___________________________________________

City: ____ Iowa City____________________________ State:___ IA__ Zip:___ 52245_______

Phone: _ 319356 5232__________________ Fax:_ 319 356 5217________________

Email: __ karin franklin@ iowa city. org__________________________________

Thank you for you assistance. Please return the completed MSWord document to Dr. John Migliaccio at drjohnmig@ aol. com or hardcopy by mail to Maturity Mark Services Co., 55 Springdale Ave., White Plains, NY 10604 2309 ( 914) 684 9112.


[Federal Register Volume 78, Number 136 (Tuesday, July 16, 2013)]
[Proposed Rules]
[Pages 42482-42484]
[FR Doc No: 2013-17020]

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

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R03-OAR-2013-0413; FRL-9834-1]

Approval and Promulgation of Air Quality Implementation Plans;
Pennsylvania; Infrastructure Requirements for the 2008 Lead National
Ambient Air Quality Standards

AGENCY: Environmental Protection Agency (EPA).

ACTION: Proposed rule.

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

SUMMARY: EPA is proposing to approve a State Implementation Plan (SIP)
revision submitted by the Commonwealth of Pennsylvania pursuant to the
Clean Air Act (CAA). Whenever new or revised national ambient air
quality standards (NAAQS) are promulgated, the CAA requires states to
submit a plan for the implementation, maintenance, and enforcement of
such NAAQS. The plan is required to address basic program elements
including, but not limited to regulatory structure, monitoring,
modeling, legal authority, and adequate resources necessary to assure
attainment and maintenance of the standards. These elements are
referred to as infrastructure requirements. The Commonwealth of
Pennsylvania made a submittal addressing the infrastructure
requirements for the 2008 lead NAAQS. This action proposes approval of
portions of the submittal. This action is being taken under the CAA.

DATES: Written comments must be received on or before August 15, 2013.

ADDRESSES: Submit your comments, identified by Docket ID Number EPA-
R03-OAR-2013-0413 by one of the following methods:

    A. www.regulations.gov. Follow the on-line instructions for
submitting comments.
    B. Email<EMAIL_ADDRESS>    C. Mail: EPA-R03-OAR-2013-0413, Cristina Fernandez, Associate
Director, Office of Air Program Planning, Air Protection Division,
Mailcode 3AP30, U.S. Environmental Protection Agency, Region III, 1650
Arch Street, Philadelphia, Pennsylvania 19103.
    D. Hand Delivery: At the previously-listed EPA Region III address.
Such deliveries are only accepted during the Docket's normal hours of
operation, and special arrangements should be made for deliveries of
boxed information.
    Instructions: Direct your comments to Docket ID No. EPA-R03-OAR-
2013-0413. EPA's policy is that all comments received will be included
in the public docket without change, and may be made available online
at www.regulations.gov, including any personal information provided,
unless the comment includes information claimed to be Confidential
Business Information (CBI) or other information whose disclosure is
restricted by statute. Do not submit information that you consider to
be CBI or otherwise protected through www.regulations.gov or email. The
www.regulations.gov Web site is an ``anonymous access'' system, which
means EPA will not know your identity or contact information unless you
provide it in the body of your comment. If you send an email comment
directly to EPA without going through www.regulations.gov, your email
address will be automatically captured and included as part of the
comment that is placed in the public docket and made available on the
Internet. If you submit an electronic comment, EPA recommends that you
include your name and other contact information in the body of your
comment and with any disk or CD-ROM you submit. If EPA cannot read your
comment due to technical difficulties and cannot contact you for
clarification, EPA may not be able to consider your comment. Electronic
files should avoid the use of special characters, any form of
encryption, and be free of any defects or viruses.
    Docket: All documents in the electronic docket are listed in the
www.regulations.gov index. Although listed in the index, some
information is not publicly available, i.e., CBI or other information
whose disclosure is restricted by statute. Certain other material, such
as copyrighted material, is not placed on the Internet and will be
publicly available only in hard copy form. Publicly available docket
materials are available either electronically in www.regulations.gov or
in hard copy during normal business hours at the Air Protection
Division, U.S. Environmental Protection Agency, Region III, 1650 Arch
Street, Philadelphia, Pennsylvania 19103. Copies of the State submittal
are available at the Pennsylvania Department of Environmental
Protection, Bureau of Air Quality Control, P.O. Box 8468, 400 Market
Street, Harrisburg, Pennsylvania 17105.

FOR FURTHER INFORMATION CONTACT: Ruth Knapp,<PHONE_NUMBER>, or by
email at<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION: On September 24, 2012, the Pennsylvania
Department of Environmental Protection (PADEP) submitted a revision to
its SIP to satisfy the requirements of section 110(a)(2) of the CAA for
the 2008 lead NAAQS.

I. Background

    On October 15, 2008, EPA substantially strengthened the primary and
secondary lead NAAQS (hereafter the ``2008 lead NAAQS''), revising the
level of the primary (health-based) standard from 1.5 micrograms per
cubic meter ([mu]g/m\3\) to 0.15 [mu]g/m\3\, measured as total
suspended particles (TSP) and not to be exceeded with an averaging time
of a rolling 3-month period. EPA also revised the secondary (welfare-
based) standard to be identical to the primary standard, as well as the
associated ambient air monitoring requirements. See 40 CFR 50.16.
    Section 110(a) of the CAA requires states to submit SIPs to provide
for the implementation, maintenance, and enforcement of a new or
revised NAAQS within three years following the promulgation of such
NAAQS or within such shorter period as EPA may prescribe. The contents
of that submission may vary depending upon the facts and circumstances.
In particular, the data and analytical tools available at the time the
state develops and submits the SIP for a new or revised NAAQS affect
the content of the submission. The contents of such SIP submissions may
also vary depending upon what provisions the state's existing SIP
already contains.
    Pursuant to section 110(a)(1) of the CAA, states are required to
submit SIPs meeting the applicable requirements of section 110(a)(2)
within three years after promulgation of a new or revised NAAQS or
within such shorter period as EPA may prescribe. Section 110(a)(1)
provides the procedural and timing requirements for SIPs and section
110(a)(2) requires states to address basic SIP elements such as
requirements for monitoring, basic program requirements and legal
authority that are designed to assure attainment and maintenance of the
NAAQS. More specifically, section 110(a)(2) lists specific elements
that states must meet for ``infrastructure'' SIP requirements related
to a newly established or revised NAAQS.
    For the 2008 lead NAAQS, states typically have met many of the
basic program elements required in CAA section 110(a)(2) through
earlier SIP submissions in connection with previous lead NAAQS.
Nevertheless, pursuant to CAA section 110(a)(1), states have to review
and revise, as appropriate, their existing lead NAAQS SIPs to ensure
that the SIPs are adequate to address the 2008 lead NAAQS. To assist
states in meeting this statutory requirement, EPA issued a guidance on
October 14, 2011, entitled, ``Guidance on Infrastructure State
Implementation Plan (SIP) Elements Required Under sections 110(a)(1)
and 110(a)(2) for the 2008 Lead (Pb) National Ambient Air Quality
Standards (NAAQS)'' (hereafter the ``2011 Lead Infrastructure
Guidance''), which lists the basic elements that states should include
in their SIPs for the 2008 lead NAAQS.

II. Summary of SIP Revision

    On September 24, 2012, PADEP provided a submittal to satisfy the
requirements of section 110(a)(2) of the CAA for the 2008 lead NAAQS.
This submittal addresses the following infrastructure elements, which
EPA is proposing to approve: CAA section 110(a)(2)(A), (B), (C),
(D)(i)(I), (D)(i)(II), (D)(ii), (E)(i), (E)(iii), (F), (G), (H), (J),
(K), (L), and (M), or portions thereof. EPA is taking separate action
on the portion of (E)(ii) as it relates to CAA section 128 (State
Boards). Pennsylvania did not submit element (I) which pertains to the
nonattainment requirements of part D, Title I of the CAA, since this
element is not required to be submitted by the 3-year submission
deadline of CAA section 110(a)(1), and will be addressed in a separate
process.
    In accordance with the decision of the U.S. Court of Appeals for
the DC Circuit, the EPA at this time is not treating the
110(a)(2)(D)(i)(I) SIP submission from the Commonwealth of Pennsylvania
as a required SIP submission. See EME Homer City Generation, LP v. EPA,
696 F.3d 7 (DC Cir. 2012), reh'g denied 2013 U.S. App. LEXIS 1623 (Jan.
24. 2013). However, even if the submission is not considered to be
``required,'' the EPA must act on the 110(a)(2)(D)(i)(I) SIP submission
from Pennsylvania because section 110(k)(2) of the CAA requires the EPA
to act on all SIP submissions. Unless the EME Homer City decision is

reversed or otherwise modified by the Supreme Court, states are not
required to submit 110(a)(2)(D)(i)(I) SIPs until the EPA has quantified
their obligations under that section. In this action, EPA is proposing
to act on the Commonwealth of Pennsylvania's 110(a)(2)(D)(i)(I)
submission.

III. Proposed Action

    EPA is proposing to approve the following section 110(a)(2)
elements of Pennsylvania's SIP revision: (A), (B), (C), (D)(i)(I),
(D)(i)(II), (D)(ii), (E)(i), (E)(iii), (F), (G), (H), (J), (K), (L),
and (M), or portions thereof. EPA will take separate action on section
110(a)(2)(E)(ii). Pennsylvania's SIP revision provides the basic
program elements specified in CAA section 110(a)(2) necessary to
implement, maintain, and enforce the 2008 lead NAAQS. This SIP revision
was submitted on September 24, 2012. This action does not include
section 110(a)(2)(I) of the CAA which pertains to the nonattainment
requirements of part D, Title I of the CAA, since this element is not
required to be submitted by the 3-year submission deadline of CAA
section 110(a)(1), and will be addressed in a separate process. EPA is
soliciting public comments on the issues discussed in this document.
These comments will be considered before taking final action.

IV. Statutory and Executive Order Reviews

    Under the CAA, the Administrator is required to approve a SIP
submission that complies with the provisions of the CAA and applicable
Federal regulations. 42 U.S.C. 7410(k); 40 CFR 52.02(a). Thus, in
reviewing SIP submissions, EPA's role is to approve state choices,
provided that they meet the criteria of the CAA. Accordingly, this
action merely proposes to approve state law as meeting Federal
requirements and does not impose additional requirements beyond those
imposed by state law. For that reason, this proposed action:
     Is not a ``significant regulatory action'' subject to
review by the Office of Management and Budget under Executive Order
12866 (58 FR 51735, October 4, 1993);
     does not impose an information collection burden under the
provisions of the Paperwork Reduction Act (44 U.S.C. 3501 et seq.);
     is certified as not having a significant economic impact
on a substantial number of small entities under the Regulatory
Flexibility Act (5 U.S.C. 601 et seq.);
     does not contain any unfunded mandate or significantly or
uniquely affect small governments, as described in the Unfunded
Mandates Reform Act of 1995 (Pub. L. 104-4);
     does not have Federalism implications as specified in
Executive Order 13132 (64 FR 43255, August 10, 1999);
     is not an economically significant regulatory action based
on health or safety risks subject to Executive Order 13045 (62 FR
19885, April 23, 1997);
     is not a significant regulatory action subject to
Executive Order 13211 (66 FR 28355, May 22, 2001);
     is not subject to requirements of Section 12(d) of the
National Technology Transfer and Advancement Act of 1995 (15 U.S.C. 272
note) because application of those requirements would be inconsistent
with the CAA; and
     does not provide EPA with the discretionary authority to
address, as appropriate, disproportionate human health or environmental
effects, using practicable and legally permissible methods, under
Executive Order 12898 (59 FR 7629, February 16, 1994).
    In addition, this proposed rule, which satisfies certain
infrastructure requirements of section 110(a)(2) of the CAA for the
2008 lead NAAQS for the Commonwealth of Pennsylvania, does not have
tribal implications as specified by Executive Order 13175 (65 FR 67249,
November 9, 2000), because the SIP is not approved to apply in Indian
country located in the state, and EPA notes that it will not impose
substantial direct costs on tribal governments or preempt tribal law.

List of Subjects in 40 CFR Part 52

    Environmental protection, Air pollution control, Incorporation by
reference, Lead, Reporting and recordkeeping requirements.

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

    Dated: July 2, 2013.
W.C. Early,
Acting Regional Administrator, Region III.
[FR Doc. 2013-17020 Filed 7-15-13; 8:45 am]
BILLING CODE 6560-50-P


From: < Johnston. Carey@ epamail. epa. gov> To: < Kenneth. N. Wood@ USA. dupont. com> Date: 4/ 5/ 2005 4: 56: 51 PM Subject: few questions regarding the DuPont Chamber Works facility in Deepwater, NJ Ken:

Re: your question:

" PS  Did not hear back from TJ Finseth re: our Titanium Dioxide plant data submittal. Have you received any feedback from him? Assume it satisfied the current request. We still plan to submit supplemental ( primarily more recent) data and are having a conference call with our plants next Monday to discuss this."

The answer is that we do not need any more information on the Dupont TiO2 plants at this time. We do, however, have a few questions regarding the DuPont Chamber Works facility in Deepwater, NJ. I would appreciate it if you could answer these questions or could forward them on to the appropriate person. Thank you.

1. Where do the discharges of chlorine, heptachlor and pendimethalin originate from? Is it from plant operations ( manufacturing processes) or from the centralized waste treatment plant? Are the pesticides coming from off site or on site wastewater?

2. Does DuPont Chambers Works report any heptachlor discharges in its DMRs?

3. What other chemicals are reported released ( to TRI or PCS/ the state) from the CWT plant?

Please send answers to:

Ms. Okemo's contact information: Audrey Okemo Audrey. Okemo@ erg. com ( 703) 633 1629 Sincerely,

Carey A. Johnston, P. E. U. S. EPA, Office of Water ph: ( 202) 566 1014 fx: ( 202) 566 1053 johnston. carey@ epa. gov CC: < Audrey. Okemo@ erg. com>, Betsy Bicknell < Betsy. Bicknell@ erg. com>, < Thomas. Finseth@ erg. com>