1 Richard_ Canady@ om b. eop. gov To: Larry Sorrels/ RTP/ USEPA/ US@ EPA cc: Edmond_ Toy@ omb. eop. gov 02/ 23/ 2004 06: 06 PM Subject: plywood Ch6 Larry,

suggested edits as discussed in call today on plywood ch 6 ( See attached file: pcwcria ch6finalomb204 rac. doc) 2 6 QUALITATIVE ASSESSMENT OF BENEFITS OF EMISSION REDUCTIONS The emission reductions achieved by this environmental regulation will provide benefits to society by improving environmental quality. This chapter provides information on the types and levels of social benefits anticipated from the plywood and composite wood products ( PCWP) NESHAP, including the health and welfare effects associated with the HAPs and other pollutants emitted by affected sources.

In general, the reduction of HAP emissions resulting from the regulation will reduce human and environmental exposure to these pollutants and thus, reduce potential adverse health and welfare effects. This chapter provides a general discussion of the various components of total benefits that may be gained from a reduction in HAPs through this NESHAP. The rule will also achieve reductions of coarse particulate matter ( PM10), volatile organic compounds ( VOC), and carbon monoxide ( CO). There will also be emissions increases in nitrogen oxides ( NOx) and sulfur dioxide ( SO2) associated with the use of incineration based controls. The benefits and disbenefits of the PM, NOx, and SO2 emissions reductions and increases are presented separately from the benefits associated with HAPs and CO. The benefits and disbenefits associated with PM, NOx, and SO2, along with the benefits associated with HAPs and CO are presented in this chapter.

6.1 Identification Of Potential Benefit Categories The benefit categories associated with the emission reductions predicted for this regulation can be broadly categorized as those benefits which are attributable to reduced exposure to HAPs, which are also VOCs, and those attributable to reduced exposure to other pollutants. Some of the HAPs associated with this regulation have been classified as probable or possible human carcinogens. As a result, one of the benefits of the regulation is a reduction in the risk of cancer. Other benefit categories include: reduced incidence of neurological effects and irritants associated with exposure to noncarcinogenic HAPs, reduced incidence of cardiovascular and central nervous system problems associated with CO. In addition to health impacts occurring as a result of reductions in HAP and CO emissions, there are welfare impacts which can also be identified. In general, welfare impacts include effects on crops and other plant life, materials damage, soiling, and acidification of estuaries. Each category is discussed separately in the following section.

6.2 Qualitative Description Of Air Related Benefits  HAPs and CO The operation of plywood and composite wood product sources produces emissions of acrolein, formaldehyde, acetaldehyde, and phenol, among other HAPs. [ why not list all of them as in 6.4? acetaldehyde, acrolein, benzene, formaldehyde, manganese, methanol, methylene chloride, and phenol?] The qualitative health and welfare benefits of these HAPs, and CO reductions are summarized separately in the discussions below. 6.2.1 Benefits of Reducing HAP Emissions According to emission estimates, the regulation will reduce approximately 11,000 tons of emissions of HAPs such as acrolein,

formaldehyde, acetaldehyde, phenol, and methanol at all affected plywood and composite wood products sources.

Human exposure to these HAPs may occur directly through inhalation or indirectly through ingestion of food or water contaminated by HAPs or through dermal exposure. HAPs may also enter terrestrial and aquatic ecosystems through atmospheric deposition. HAPs can be deposited on vegetation and soil through wet or dry deposition. HAPs may also enter the aquatic environment from the atmosphere via gas exchange between surface water and the ambient air, wet or dry deposition of particulate HAPs and particles to which HAPs adsorb, and wet or dry deposition to watersheds with subsequent leaching or runoff to bodies of water. 1 This analysis is focused only on the air quality benefits of HAP reduction. <IP_ADDRESS> Health Benefits of Reduction in HAP Emissions.

The HAP emission reductions achieved by this rule are expected to reduce exposure to ambient concentrations of acrolein, formaldehyde,

acetaldehyde, and phenol, [ why not list all used in 6.4  acetaldehyde, acrolein, benzene, formaldehyde, manganese, methanol, methylene chloride,

and phenol ?] which will reduce a variety of adverse health effects considering both cancer and noncancer endpoints. Acrolein is classified as a possible human carcinogen, according to the Integrated Risk Information System ( IRIS) 13, an EPA system for classifying chemicals by cancer risk.

This means that there is some evidence to indicate that exposure to this chemical could cause an increased risk of cancer in humans. Acrolein may also cause general respiratory congestion and upper respiratory tract irritation. Formaldehyde and acetaldehyde are classified as probable human carcinogens, according to IRIS. Therefore, a reduction in human exposure to acrolein, formaldehyde, and acetaldehyde could lead to a decrease in cancer risk and ultimately to a decrease in cancer mortality.

The remaining HAP emitted by plywood and composite wood products sources, phenol and methanol, have not been shown to cause cancer. However, exposure to these pollutants may still result in adverse health impacts to human and non human populations. In particular,

methanol has been shown to be an irritant causing dizziness, headaches, and slight visual impairment.

For the HAPs covered by the NESHAP, evidence on the potential toxicity of the pollutants varies. However, given sufficient exposure conditions, each of these HAPs has the potential to elicit adverse health or environmental effects in the exposed populations. It can be expected that emission reductions achieved through the NESHAP will decrease the incidence of these adverse health effects.

<IP_ADDRESS> Welfare Benefits of Reduction in HAP Emissions.

The welfare effects of exposure to HAPs have received less attention from analysts than the health effects. However, this situation is changing, especially with respect to the effects of toxic substances on ecosystems. Over the past ten years, ecotoxicologists have started to build models of ecological systems which focus on interrelationships in function, the dynamics of stress, and the adaptive potential for recovery. This is consistent with the observation that chronic sub lethal exposures may affect the normal functioning of individual species in ways that make it less than competitive and therefore more susceptible to a variety of factors including disease, insect attack, and decreases in habitat quality. 15 All of these factors may contribute to an overall change in the structure ( i. e., composition) and function of the ecosystem. 5 The adverse, non human biological effects of HAP emissions include ecosystem and recreational and commercial fishery impacts. Atmospheric deposition of HAPs directly to land may affect terrestrial ecosystems. Atmospheric deposition of HAPs also contributes to adverse aquatic ecosystem effects. This not only has adverse implications for individual wildlife species and ecosystems as a whole, but also the humans who may ingest contaminated fish and waterfowl. In general, HAP emission reductions achieved through the NESHAP should reduce the associated adverse environmental impacts.

6.2.2 Benefits of Reduced CO Emissions Due to HAP Controls As is mentioned above, controls that will be required on plywood and composite wood products sources to reduce HAPs will also reduce emissions of CO. The EPA Staff Paper for CO provides a summary of the health effects information pertinent to the NAAQS for CO16. This information is a summary of information from the CO Criteria Document ( CD) 17, which provides a critical review of a wide variety of health effects studies, including a limited number of newer health effects studies, as well as older studies. Some were conducted at extremely high levels of CO ( i. e. much higher than typically found in ambient air); however, the focus of this Staff Paper is on those key controlled exposure laboratory studies and newer epidemiology studies, which were conducted with human subjects at COHb levels that are most relevant to regulatory decision making.

Based on the CD, staff concludes that human health effects associated with exposure to CO include cardiovascular system and central nervous system ( CNS) effects. In addition, consideration is given in the CD to combined exposure to CO, other pollutants, drugs, and the influence of environmental factors. Cardiovascular effects of CO are directly related to reduced oxygen content of blood caused by combination of CO with Hb to form COHb, resulting in tissue hypoxia. Most healthy individuals have mechanisms ( e. g. increased blood flow, blood vessel dilation) which compensate for this reduction in tissue O2, although the effect of reduced maximal exercise capacity has been reported in healthy persons at low COHb levels. Several other medical conditions such as occlusive vascular disease, chronic obstructive lung disease, and anemia can increase susceptibility to potential adverse effects of CO during exercise.

Effects of CO on the CNS involve both behavioral and physiological changes. These include modification of visual perception, hearing, motor and sensorimotor performance, vigilance, and cognitive ability. Developmental toxicity effects of low level ambient CO exposures, though not well studied in humans, may pose a threat to the fetus. Finally, environmental factors ( e. g. altitude, temperature), drug interaction, and pollutant interaction also can play a role in the public health impact of ambient CO exposure. There is little new information on these effects.

Exhibit 6 2 is a summary of key health effects and studies which have been identified as being most pertinent to a regulatory decision on the NAAQS for CO18. Each of the key studies is considered in light of limitations discussed in the CD and the Staff Paper. For example, epidemiological studies are limited by factors such as exposure uncertainties and confounding variables, and many of the controlled exposure studies of CO health effects have been hampered by uncertainties regarding COHb measurements, relatively small sample sizes, and lack of " real world" exposure conditions. Exhibit " 6 2 Key Health Effects of Exposure to Ambient Carbon Monoxide Target Organ Health Effectsa, b Tested Populationc References Lungs Reduced maximal exercise duration with 1 h peak CO exposures resulting in

2.3% COHb ( GC) Healthy individuals Drinkwater et al. ( 1974)

Raven et al. ( 1974b)

Horvath et al. ( 1975)

Heart Reduced time to ST segment change of the ECG ( earlier onset of myocardial ischemia) with peak CO exposures resulting in

2.4% COHb ( GC) Individuals with coronary artery disease Allred et al. ( 1989a, b;

1991)

Heart Reduced exercise duration because of increased chest pain ( angina) with peak CO exposures resulting in

3% COHb ( CO Ox) Individuals with coronary artery disease Anderson et al. ( 1973)

Sheps et al. ( 1987)

Adams et al. ( 1988)

Kleinman et al. ( 1989,

1998*)

Allred et al. ( 1989a, b;

1991)

Heart Increased number and complexity of arrhythmia ( abnormal heart rhythm) with peak CO exposures resulting in

6% COHb ( CO Ox) Individuals with coronary artery disease and high baseline ectopy ( chronic arrhythmia) Sheps et al. ( 1990)

Heart Increased hospital admissions associated with ambient pollutant exposures Individuals > 65 years old with cardiovascular disease Schwartz and Morris ( 1995*)

Morris et al. ( 1995*)

Schwartz ( 1997*)

Burnett et al. ( 1997*)

Brain Central nervous system effects, such as decrements in hand eye coordination ( driving or tracking) and in attention or vigilance ( detection of infrequent events), with 1 h peak CO exposures (  5 to 20% COHb) Healthy individuals Horvath et al. ( 1971)

Fodor and Winneke ( 1972)

Putz et al. ( 1976, 1979)

Benignus et al. ( 1987) aThe EPA has set significant harm levels of 50 ppm ( 8 h average), 75 ppm ( 4 h average), and 125 ppm ( 1 h average). Exposure under these conditions could result in COHb levels of 5 to 10% and cause significant health effects in sensitive individuals.

bMeasured blood COHb level after CO exposure.

cFetuses, infants, pregnant women, elderly people, and people with anemia or with a history of cardiac or respiratory disease may be particularly sensitive to CO.

dThis table is a reproduction of Table 6 7 of the CD ( p. 6 36, U. S. EPA, 1999a).

* Newer studies, published since completion of the last CO NAAQS review. Although acute poisoning induced by CO can be lethal and is probably the best known health endpoint of CO, this only occurs at very high concentrations of CO ( greater than 100 ppm, hourly average), which are not pertinent to the setting of the NAAQS. In the ambient air,

exposures to lower levels of CO predominate. [ these are the occupational limits   why are they being presented as ambient?] Very little data are available demonstrating human health effects in healthy individuals caused by or associated with exposures to low CO concentrations.

Decrements in maximal exercise duration and performance in healthy individuals have been reported at COHb levels of > 2.3% an d > 4.3% ( GC),

respectively; however, these decrements are small and likely to affect only athletes in competition. No effects were seen in healthy individuals during submaximal exercise, representing more typical daily activities, at levels as high as 15 to 20 % COHb20. Most recent evidence of CNS effects induced by exposure to CO indicates that behavioral impairments in healthy individuals should not be expected until COHb levels exceed 20% ( CO Ox), well above what would be caused by typical ambient air levels of CO21. Evidence of CO induced fetal toxicity or of interactions with high altitudes, drugs, other pollutants, or other environmental stresses remains uncertain or suggests that effects of concern will occur in healthy individuals only with exposure to much higher levels of CO than are likely for offsite receptors for these facilities22.

6.3 Qualitative Description of Effects from Reductions and Increases in Emissions from Other Pollutants Due to HAP Controls As is mentioned above, controls that will be required on PCWP sources to reduce HAPs will also reduce emissions of other pollutants,

namely: PM10, PM2.5, and increase NOx and SO2 emissions. For more information on these non HAP emissions and emission reductions, please refer to Chapter 3 of this RIA, the preamble for this rule, and the docket. The effects associated with exposure to PM ( both coarse and fine), NOx,

and SO2 emissions are presented below. 9 6.3.1 Effects of NOx Emissions.

Emissions of NOx produce a wide variety of health and welfare effects. Nitrogen dioxide can irritate the lungs at high occupational levels and may lower resistance to respiratory infection, although the research has been equivocal. NOx emissions are an important precursor to acid rain and may affect both terrestrial and aquatic ecosystems. Atmospheric deposition of nitrogen leads to excess nutrient enrichment problems (" eutrophication") in the Chesapeake Bay and several nationally important estuaries along the East and Gulf Coasts. Eutrophication can produce multiple adverse effects on water quality and the aquatic environment, including increased algal blooms, excessive phytoplankton growth, and low or no dissolved oxygen in bottom waters. Eutrophication also reduces sunlight, causing losses in submerged aquatic vegetation critical for healthy estuarine ecosystems. Deposition of nitrogen containing compounds also affects terrestrial ecosystems. Nitrogen fertilization can alter growth patterns and change the balance of species in an ecosystem.

Nitrogen dioxide and airborne nitrate also contribute to pollutant haze ( often brown in color), which impairs visibility and can reduce residential property values and the value placed on scenic views.

NOx in combination with volatile organic compounds ( VOC) also serves as a precursor to ozone. Based on a large number of recent studies, EPA has identified several key health effects that may be associated with exposure to elevated levels of ozone. Exposures to ambient ozone concentrations have been linked to increased hospital admissions and emergency room visits for respiratory problems. Repeated exposure to ozone may increase susceptibility to respiratory infection and lung inflammation and can aggravate preexisting respiratory disease, such as asthma. Repeated prolonged exposures ( i. e., 6 to 8 hours) to ozone at levels between 0.08 and 0.12 ppb, over months to years may lead to repeated inflammation of the lung, impairment of lung defense mechanisms, and irreversible changes in lung structure, which could in turn lead to premature aging of the lungs and/ or chronic respiratory illnesses such as emphysema, chronic bronchitis, and asthma.

Children have the highest exposures to ozone because they typically are active outside playing and exercising, during the summer when ozone levels are highest. Further, children are more at risk than adults from the effects of ozone exposure because their respiratory systems are still developing. Adults who are outdoors and moderately active during the summer months, such as construction workers and other outdoor workers, also are among those with the highest exposures. These individuals, as well as people with respiratory illnesses such as asthma, especially children with asthma, may experience reduced lung function and increased respiratory symptoms, such as chest pain and cough, when exposed to relatively low ozone levels during periods of moderate exertion. In addition to human health effects, ozone adversely affects crop yield, vegetation and forest growth, and the durability of materials. Ozone causes noticeable foliar damage in many crops, trees, and ornamental plants ( i. e., grass, flowers, shrubs, and trees) and causes reduced growth in plants.

Particulate matter ( PM) can also be formed from NOx emissions. Secondary PM is formed in the atmosphere through a number of physical and chemical processes that transform gases such as NOx, SO2, and VOC into particles. A discussion of the effects of PM on human health and the environment are discussed further below. Overall, emissions of NOx from PCWP sources can lead to some of the effects discussed in this section  either those directly related to NOx emissions, or the effects of ozone and PM 10 resulting from the combination of NOx with other pollutants.

6.3.2 Benefits of PM Reductions.

Scientific studies have linked PM ( alone or in combination with other air pollutants) with a series of health effects ( EPA, 1996). Fine particles ( PM2.5) can penetrate deep into the lungs to contribute to a number of the health effects. These health effects include decreased lung function and alterations in lung tissue and structure and in respiratory tract defense mechanisms which may be manifest in increased respiratory symptoms and disease or in more severe cases, increased hospital admissions and emergency room visits or premature death. Children, the elderly, and people with cardiopulmonary disease, such as asthma, are most at risk from these health effects.

PM also causes a number of adverse effects on the environment. Fine PM is the major cause of reduced visibility in parts of the U. S., including many of our national parks and wilderness areas. Other environmental impacts occur when particles deposit onto soil, plants, water, or materials. For example, particles containing nitrogen and sulfur that deposit onto land or water bodies may change the nutrient balance and acidity of those environments, leading to changes in species composition and buffering capacity. Particles that are deposited directly onto leaves of plants can, depending on their chemical composition, corrode leaf surfaces or interfere with plant metabolism. Finally, PM causes soiling and erosion damage to materials.

Thus, reducing the emissions of PM and PM precursors from PCWP sources can help to improve some of the effects mentioned above  either those related to primary PM emissions, or the effects of secondary PM generated by the combination of NOx or SO2 with other pollutants in the atmosphere.

6.3.3 Effects of SO2 Emissions.

Very high concentrations of sulfur dioxide ( SO2) affect breathing and ambient levels have been hypothesized to aggravate existing respiratory and cardiovascular disease. Potentially sensitive populations include asthmatics, individuals with bronchitis or emphysema, children and the elderly. SO2 is also a primary contributor to acid deposition, or acid rain, which causes acidification of lakes and streams and can damage trees, crops, historic buildings and statues. In addition, sulfur compounds in the air contribute to visibility impairment in large parts of the country. This is especially noticeable in national parks.

PM can also be formed from SO2 emissions. Secondary PM is formed in the atmosphere through a number of physical and chemical processes that transform gases, such as SO2, into particles. Overall, emissions of SO2 can lead to some of the effects discussed in this section  either those directly related to SO2 emissions, or the effects of ozone and PM resulting from the combination of SO2 with other pollutants.

6.4 Lack Of Approved Methods To Quantify HAP Benefits 11 The most significant effect associated with the HAPs that are controlled with the rule is the potential incidence of cancer. In previous analyses of the benefits of reductions in HAPs, EPA has quantified and monetized the benefits of potential reductions in the incidences of cancer 23, 24. In some cases, EPA has also quantified ( but not monetized) reductions in the number of people exposed to noncancer HAP risks above no effect levels25.

Monetization of the benefits of reductions in cancer incidences requires several important inputs, including central estimates of cancer risks, estimates of exposure to carcinogenic HAPs, and estimates of the value of an avoided case of cancer ( fatal and non fatal). In the above referenced analyses, EPA relied on unit risk factors ( URF) developed through risk assessment procedures. The unit risk factor is a quantitative estimate of the carcinogenic potency of a pollutant, often expressed as the probability of contracting cancer from a 70 year lifetime continuous exposure to a concentration of one

g/ m3 of a pollutant. These URFs are designed to be conservative, and as such, are more likely to represent the high end of the distribution of risk rather than a best or most likely estimate of risk.

In a typical analysis of the expected health benefits of a regulation ( e. g., the Heavy Duty Engine / Diesel Fuel Regulatory Impact Analysis), health effects are estimated by applying changes in pollutant concentrations to best estimates of risk obtained from epidemiological studies. As the purpose of a benefit analysis is to describe the benefits most likely to occur from a reduction in pollution, use of highend conservative risk estimates will over estimate the expected benefits of the regulation. For this reason, we will not attempt to quantify the health benefits of reductions in HAPs unless best estimates of risks are available. While we used high end risk estimates in past analyses, recent advice from the EPA Science Advisory Board ( SAB) and internal methods reviews have suggested that we avoid using highend estimates in current analyses. EPA is working with the SAB to develop better methods for analyzing the benefits of reductions in HAPs.

While not appropriate for inclusion in our primary quantified benefits analysis, to estimate the potential baseline risks posed by the PCWP source category and the potential impact of applicability cutoffs, EPA performed a " rough" risk assessment for 185 of the 223 facilities in the PCWP source category. There are large uncertainties regarding all components of the risk quantification step, including location of emission reductions, emission estimates, air concentrations, exposure levels and dose response relationships. However, if these uncertainties are properly identified and characterized, it is possible to provide upper bound estimates of the potential reduction in inhalation cancer incidence associated with this rule. It is important to keep in mind that these estimates will not cover non inhalation based cancer risks and non cancer health effects.

The HAP included in this " rough" risk assessment were acetaldehyde, acrolein, benzene, formaldehyde, manganese, methanol, methylene chloride, and phenol. Of these HAP, four are presently not considered to have thresholds: acetaldehyde, benzene, formaldehyde, and methylene chloride.

Of the 185 facilities assessed, 148 facilities were found to pose cancer risks equal to or greater than 1 in 1,000,000 to their surrounding population. Forty six facilities were predicted to pose cancer risks of 1 in 100,000 or greater, and two PCWP facilities were found to pose cancer risks equal to or greater than 1 in 10,000.

If this rule is implemented at all PCWP facilities, annual cancer incidence would be reduced from 12 about 0.09 cases/ year to about 0.02 cases/ year, while the number of people at or above a cancer risk level of 1 in a million would be reduced from about 900,000 to 150,000. The HAP contributing the greatest to this estimate were . In addition, the number of people exposed to hazard index ( HI) values equal to or greater than 1 was estimated to be reduced from about 270,000 to about 30,000. The HAP contributing the greatest to this estimate were . ( Details of these analyses are available in the docket). EPA has not tried to monetize this reduced incidence of inhalation cancer for several important technical reasons. The primary reasons include the lack of information on the latency period for the onset of the disease and the fact that we have no information on the proportion of fatal versus nonfatal cancers which may occur. These factors prevent us from providing monetized estimates.

For non cancer health effects, previous analyses have estimated changes in populations exposed above the reference concentration level ( RfC). However, this requires estimates of populations exposed to HAPs from controlled sources. Due to data limitations, we do not have sufficient information on emissions from specific sources and thus are unable to model changes in population exposures to ambient concentrations of HAPs above the RfC. As a result, we are unable to place a monetary value of the HAP related benefits associated with this rule.

6.5 Summary The HAPs that are reduced as a result of implementing the plywood and composite wood products NESHAP will produce a variety of benefits, some of which include: a possible reduction in the incidence of cancer to exposed populations, neurotoxicity, irritation, and crop or plant damage. The rule will also produce benefits associated with reductions in CO. Human health effects associated with exposure to CO include cardiovascular system and central nervous system ( CNS) effects. Although we are unable to place a monetary value on these benefits, the information on the variety of effects associated with these pollutants and the level of reductions anticipated from the NESHAP indicate that the benefits of the rule will be substantial. 13 6.6 REFERENCES 1. U. S. Environmental Protection Agency. Regulatory Impact Analysis for the National Emissions Standards for Hazardous Air Pollutants for Source Categories: Organic Hazardous Air Pollutants from the Synthetic Organic Chemical Manufacturing Industry and Seven Other Processes. Draft Report. Office of Air Quality Planning and Standards. Research Triangle Park, NC. EPA 450/ 3 92 009. December 1992.

2. Mathtech, Inc. Benefit Analysis Issues for Section 112 Regulations. Final report prepared for U. S. Environmental Protection Agency. Office of Air Quality Planning and Standards. Contract No. 68 D8 0094. Research Triangle Park, NC. May 1992.

3. U. S. Environmental Protection Agency. Cancer Risk from Outdoor Exposure to Air Toxics. Volume I. EPA 450/ 1 90 004a. Office of Air Quality Planning and Standards. Research Triangle Park, NC. September 1990.

4. Graham, John D., D. R. Holtgrave, and M. J. Sawery. " The Potential Health Benefits of Controlling Hazardous Air Pollutants." In: Health Benefits of Air Pollution Control: A Discussion. Blodgett, J. ( ed). Congressional Research Service report to Congress. CR589 161. Washington, DC. February 1989.

5. Reference 4.

6. Voorhees, A., B. Hassett, and I. Cote. Analysis of the Potential for Non Cancer Health Risks Associated with Exposure to Toxic Air Pollutants. Paper presented at the 82nd Annual Meeting of the Air and Waste Management Association. 1989.

7. Reference 4.

8. Reference 6.

9. Cote, I., L. Cupitt and B. Hassett. Toxic Air Pollutants and Non Cancer Health Risks. Unpublished paper provided by B. Hassett. 1988.

10. NAS. Chlorine and Hydrogen Chloride. National Academy of Sciences, National Research Council. Chapter 7. 1975.

11. Stern, A. et al. Fundamentals of Air Pollution. Academic Press, New York. 1973.

12. Weinstein, D. and E. Birk. The Effects of Chemicals on the Structure of Terrestrial Ecosystems: Mechanisms and Patterns of Change. In: Levin, S. et al. ( eds). Ecotoxicology: Problems and Approaches. Chapter 7. pp. 181 209. Springer Verlag, New York. 1989.

13. U. S. Environmental Protection Agency. Integrated Risk Information System; website access available at www. epa. gov/ ngispgm3/ iris. 14. Reference 1. p. 3 5.

14. Reference 1. pp. 8 4 to 8 5.

15. U. S. Environmental Protection Agency. Ecological Exposure and Effects of Airborne Toxic Chemicals: An Overview. EPA/ 6003 91/ 001. Environmental Research Laboratory. Corvallis, OR. 1991.

16. U. S. Environmental Protection Agency; Staff Paper for the Carbon Monoxide NAAQS; Office of Air Quality Planning and Standards, Research Triangle Park, N. C.; 2000.

17. U. S. Environmental Protection Agency; Criteria Document for Carbon Monoxide; Office of Air Quality Planning and Standards, Research Triangle Park, N. C.; 1999.

18. Reference 17 at Section 6.9.

19. Reference 18.

20. Reference 18.

21. Reference 18.

22. Reference 18.

23. U. S. Environmental Protection Agency. 1992. Draft Regulatory Impact Analysis of National Emissions Standards for Hazardous Air Pollutants for By Product Coke Oven Charging, Door Leaks, and Topside Leaks. Office of Air Quality Planning and Standards, Research Triangle Park, NC.

24. U. S. Environmental Protection Agency. 1995. Regulatory Impact Analysis for the Petroleum Refinery NESHAP. Revised Draft for Promulgation. Office of Air Quality Planning and Standards, Research Triangle Park, NC.

25. Reference 24.


[Federal Register Volume 78, Number 36 (Friday, February 22, 2013)]
[Notices]
[Pages 12331-12334]
[FR Doc No: 2013-04059]

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DEPARTMENT OF HEALTH AND HUMAN SERVICES

Food and Drug Administration

[Docket No. FDA-2013-N-0001]

Request for Nominations for Voting and/or Nonvoting Consumer
Representatives on Public Advisory Committees or Panels and Request for
Notification From Consumer Organizations Interested in Participating in
the Selection Process for Nominations for Voting and/or Nonvoting
Consumer Representatives on Public Advisory Committees or Panels

AGENCY: Food and Drug Administration, HHS.

ACTION: Notice.

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

SUMMARY: The Food and Drug Administration (FDA) is requesting that any
consumer organizations interested in participating in the selection of
voting and/or nonvoting consumer representatives to serve on its
advisory committees or panels notify FDA in writing. FDA is also
requesting nominations for voting and/or nonvoting consumer
representatives to serve on advisory committees and/or panels for which
vacancies currently exist or are expected to occur in the near future.
Nominees recommended to serve as a voting or nonvoting consumer
representative may either be self-nominated or may be nominated by a
consumer organization. Nominations will be accepted for current
vacancies and for those that will or may occur through December 2013.

DATES: Any consumer organization interested in participating in the
selection of an appropriate voting or nonvoting member to represent
consumer interests on an FDA advisory committee or panel may send a
letter or email stating that interest to FDA by March 25, 2013, for
vacancies listed in this notice. Concurrently, nomination materials for
prospective candidates should be sent to FDA by March 25, 2013.

ADDRESSES: All statements of interest from consumer organizations
interested in participating in the selection process and consumer
representative nominations should be sent electronically to
<EMAIL_ADDRESS>by mail to Advisory Committee Oversight and Management
Staff, 10903 New Hampshire Ave., Bldg. 32, rm. 5129, Silver Spring, MD
20993-0002, or by fax to<PHONE_NUMBER>. Information about becoming a
member of an FDA advisory committee can be obtained by visiting FDA's
Web site at http://www.fda.gov/AdvisoryCommittees/default.htm.

FOR FURTHER INFORMATION CONTACT:  Dornette Spell-LeSane, Advisory
Committee Oversight and Management Staff, Food and Drug Administration,
10903 New Hampshire Ave., Bldg. 32, rm. 5129, Silver Spring, MD 20993-
0002,<PHONE_NUMBER><EMAIL_ADDRESS>    For questions relating to specific advisory committees or panels,
contact the appropriate person listed in table 1 in the SUPPLEMENTARY
INFORMATION section of this document.

SUPPLEMENTARY INFORMATION:
    For questions relating to specific advisory committees or panels,
contact the appropriate person listed in table 1 of this document.

                                      Table 1--Advisory Committee Contacts
----------------------------------------------------------------------------------------------------------------
                  Contact person                                           Committee/panel
----------------------------------------------------------------------------------------------------------------
Diane Goyette, Center for Drug Evaluation and       Anti-Infective Drugs.
 Research, Food and Drug Administration, 10903 New
 Hampshire Ave., Bldg. 31, Rm. 2408, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER>, FAX: 301-847-
 8533<EMAIL_ADDRESS>

Kristina Toliver, Center for Drug Evaluation and    Cardiovascular and Renal Drugs.
 Research, Food and Drug Administration, 10903 New
 Hampshire Ave., Bldg. 31, Rm. 2408, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER>, FAX: 301-847-
 8533<EMAIL_ADDRESS>Diem-Kieu Ngo, Center for Drug Evaluation and       Endocrinologic and Metabolic Drugs.
 Research, Food and Drug Administration, 10903 New
 Hampshire Ave., Bldg. 31, Rm. 2408, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER> X9021, FAX:
<PHONE_NUMBER><EMAIL_ADDRESS>Glendolynn Johnson, Center for Drug Evaluation and  Nonprescription Drugs and Peripheral and Central Nervous
 Research, Food and Drug Administration, 10903 New   System Drugs.
 Hampshire Ave., Bldg. 31, Rm. 2434, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER>, FAX: 301-847-
 8533<EMAIL_ADDRESS>Cindy Hong, Center for Drug Evaluation and          Pulmonary Allergy Drugs.
 Research, Food and Drug Administration, 10903 New
 Hampshire Ave., Bldg. 31, Rm. 2528, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER>, FAX: 301-847-
 8533<EMAIL_ADDRESS>Karen Strambler, Center for Food Safety and         Food Advisory Committee.
 Applied Nutrition, Food and Drug Administration,
 5100 Paint Branch Pkwy., Rm. 1C016, College Park,
 MD 20740,<PHONE_NUMBER>, FAX:<PHONE_NUMBER>.
<EMAIL_ADDRESS>Donald Jehn, Center for Biologics Evaluation and    Vaccines and Related Biological Products.
 Research, 1401 Rockville Pike (HFM-71),
 Rockville, MD 20852,<PHONE_NUMBER>, FAX: 301-827-
 0294<EMAIL_ADDRESS>Jamie Waterhouse, Center for Devices and            Circulatory System Devices and Ear, Nose and Throat Devices
 Radiological Devices, Food and Drug                 Panel.
 Administration, 10903 New Hampshire Ave., Bldg.
 66, Rm. 1611, Silver Spring, MD 20993-0002, 301-
 796-3063, FAX:<PHONE_NUMBER>,
<EMAIL_ADDRESS>Shanika Craig, Center for Devices and Radiological  Microbiology Devices Panel.
 Devices, Food and Drug Administration, 10903 New
 Hampshire Ave., Bldg. 66, Rm. 1613, Silver
 Spring, MD 20993-0002,<PHONE_NUMBER>, FAX: 301-847-
 8121<EMAIL_ADDRESS>Sara J. Anderson, Center for Devices and            Orthopaedic and Rehabilitation Devices Panel.
 Radiological Health, 10903 New Hampshire Ave.,
 Bldg. 66, Rm. 1544, Silver Spring, MD 20903, 301-
 796-7047, FAX:<PHONE_NUMBER>,
<EMAIL_ADDRESS>----------------------------------------------------------------------------------------------------------------

    FDA is requesting nominations for voting and/or nonvoting consumer
representatives for the vacancies listed in table 2 of this document:

                                       Table 2--Committee/Panel Vacancies
----------------------------------------------------------------------------------------------------------------
                                                      Current and  upcoming
     Committee/panel/areas of expertise needed              vacancies               Approximate date needed
----------------------------------------------------------------------------------------------------------------
Anti-Infective Drugs..............................  1-Voting.................  December 1, 2013.
    Knowledgeable in the fields of infectious
     disease, internal medicine, microbiology,
     pediatrics, epidemiology or statistics, and
     related specialties
Cardiovascular and Renal Drugs....................  1-Voting.................  July 1, 2013.
    Knowledgeable in the fields of cardiology,
     hypertension, arrhythmia, angina, congestive
     heart failure, diuresis, and biostatistics.
Endocrinologic and Metabolic Drugs................  1-Voting.................  July 1, 2013.
    Reviews and evaluates data concerning the
     safety and efficacy of marketed and
     investigational human drugs products for use
     in the treatment of endocrine and metabolic
     disorders.
Nonprescription Drugs.............................  1-Voting.................  July 1, 2013.
    Knowledgeable in the fields of internal
     medicine, family practice, clinical
     toxicology, clinical pharmacology, pharmacy,
     dentistry, and related specialties.
Peripheral and Central Nervous System Drugs.......  1-Voting.................  Immediately.
    Knowledgeable in the fields of neurology,
     neuropharmacology, neuropathology,
     otolaryngology, epidemiology or statistics,
     and related specialties
Pulmonary Allergy Drugs...........................  1-Voting.................  June 1, 2013.
    Knowledgeable in the fields of pulmonary
     medicine, allergy, clinical immunology, and
     epidemiology or statistics
Food Committee....................................  1-Voting.................  July 1, 2013.
    Knowledgeable in the areas of food technology,
     pediatric development, nutrition, food
     microbiology and toxicology
Vaccines and Related Biological Products..........  1-Voting.................  Immediately.
    Knowledgeable in the fields of immunology,
     molecular biology, rDNA, virology,
     bacteriology, epidemiology or biostatistics,
     allergy, preventive medicine, infectious
     diseases, pediatrics, microbiology, and
     biochemistry
Circulatory System Devices Panel..................  1-Nonvoting..............  July 1, 2013.
    Knowledgeable in the safety and effectiveness
     of marked and investigational devices for use
     in the circulatory and vascular systems.
Ear, Nose, and Throat Devices Panel...............  1-Nonvoting..............  Immediately.
    Knowledgeable in the safety and effectiveness
     of marketed and investigational ear, nose and
     throat devices
Microbiology Devices Panel........................  1-Nonvoting..............  Immediately.

    Knowledgeable in data concerning the safety
     and effectiveness of marketed and
     investigational in vitro devices for use in
     clinical laboratory medicine including
     microbiology, virology, and infectious
     disease and makes appropriate recommendations
Orthopaedic and Rehabilitation Devices Panel......  1-Nonvoting..............  September 1, 2013.
    Knowledgeable in data concerning the safety
     and effectiveness of marketed and
     investigational orthopaedic and
     rehabilitation devices
----------------------------------------------------------------------------------------------------------------

I. Functions

A. Anti-Infective Drugs

    The committee reviews and evaluates available data concerning the
safety and effectiveness of marketed and investigational human drug
products for use in the treatment of infectious diseases and disorders
and makes appropriate recommendations to the Commissioner of Food and
Drugs.

B. Cardiovascular and Renal Drugs

    The Committee reviews and evaluates available data concerning the
safety and effectiveness of marketed and investigational human drug
products for use in the treatment of cardiovascular and renal disorders
and makes appropriate recommendations to the Commissioner of Food and
Drugs.

B. Endocrinologic and Metabolic Drugs

    The Committee reviews and evaluates data concerning the safety and
effectiveness of marketed and investigational human drug products for
use in the treatment of endocrine and metabolic disorders and makes
appropriate recommendations to the Commissioner of Food and Drugs.

C. Nonprescription Drugs

    The Committee reviews and evaluates available data concerning the
safety and effectiveness of over-the-counter (nonprescription) human
drug products, or any other FDA-regulated product, for use in the
treatment of a broad spectrum of human symptoms and diseases and
advises the Commissioner of Food and Drugs either on the issuance of
monographs establishing conditions under which these drugs are
generally recognized as safe and effective and not misbranded or on the
approval of new drug applications for such drugs. The Committee will
serve as a forum for the exchange of views regarding the prescription
and nonprescription status, including switches from one status to
another, of these various drug products and combinations thereof. The
Committee may also conduct peer review of Agency sponsored intramural
and extramural scientific biomedical programs in support of FDA's
mission and regulatory responsibilities.

D. Peripheral and Central Nervous system Drugs

    The Committee reviews and evaluates data concerning the safety and
effectiveness of marketed and investigational human drug products for
use in the treatment of neurologic diseases and makes appropriate
recommendations to the Commissioner of Food and Drugs.

E. Pulmonary Allergy Drugs

    The Committee reviews and evaluates available data concerning the
safety and effectiveness of marketed and investigational human drug
products for use in the treatment of pulmonary disease and diseases
with allergic and/or immunologic mechanisms and makes appropriate
recommendations to the Commissioner of Food and Drugs.

F. Food Advisory Committee

    The Committee provides advice to the Commissioner of Food and Drugs
and other appropriate officials, on emerging food safety, food science,
nutrition, and other food-related health issues that FDA considers of
primary importance for its food and cosmetics programs. The Committee
may be charged with reviewing and evaluating available data and making
recommendations on matters such as those relating to: (1) Broad
scientific and technical food or cosmetic related issues, (2) the
safety of new foods and food ingredients, (3) labeling of foods and
cosmetics, (4) nutrient needs and nutritional adequacy, and (5) safe
exposure limits for food contaminants. The Committee may also be asked
to provide advice and make recommendations on ways of communicating to
the public the potential risks associated with these issues and on
approaches that might be considered for addressing the issues.

G. Vaccines and Related Biologic Products

    The Committee reviews and evaluates data concerning the safety,
effectiveness, and appropriate use of vaccines and related biological
products which are intended for use in the prevention, treatment, or
diagnosis of human diseases, and, as required, any other products for
which FDA has regulatory responsibility. The Committee also considers
the quality and relevance of FDA's research program which provides
scientific support for the regulation of these products and makes
appropriate recommendations to the Commissioner of Food and Drugs.

H. Certain Panels of the Medical Devices Advisory Committee

    The Committee reviews and evaluates data on the safety and
effectiveness of marketed and investigational devices and makes
recommendations for their regulation. With the exception of the Medical
Devices Dispute Resolution Panel, each panel, according to its
specialty area; advises on the classification or reclassification of
devices into one of three regulatory categories; advises on any
possible risks to health associated with the use of devices; advises on
formulation of product development protocols; reviews premarket
approval applications for medical devices; reviews guidelines and
guidance documents; recommends exemption of certain devices from the
application of portions of the Federal Food, Drug, and Cosmetic Act;
advises on the necessity to ban a device; and responds to requests from
the Agency to review and make recommendations on specific issues or
problems concerning the safety and effectiveness of devices. With the
exception of the Medical Devices Dispute Resolution Panel, each panel,
according to its specialty area, may also make appropriate
recommendations to the Commissioner of Food and Drugs on issues
relating to the design of clinical studies regarding

the safety and effectiveness of marketed and investigational devices.

II. Criteria for Members

    Persons nominated for membership as consumer representatives on the
committees or panels should meet the following criteria: (1)
Demonstrate ties to consumer and community-based organizations, (2) be
able to analyze technical data, (3) understand research design, (4)
discuss benefits and risks, and (5) evaluate the safety and efficacy of
products under review. The consumer representative should be able to
represent the consumer perspective on issues and actions before the
advisory committee; serve as a liaison between the committee and
interested consumers, associations, coalitions, and consumer
organizations; and facilitate dialogue with the advisory committees on
scientific issues that affect consumers.

III. Selection Procedures

    Selection of members representing consumer interests is conducted
through procedures that include the use of organizations representing
the public interest and public advocacy groups. These organizations
recommend nominees for the Agency's selection. Representatives from the
consumer health branches of Federal, State, and local governments also
may participate in the selection process. Any consumer organization
interested in participating in the selection of an appropriate voting
or nonvoting member to represent consumer interests should send a
letter stating that interest to FDA (see ADDRESSES) within 30 days of
publication of this document.
    Within the subsequent 30 days, FDA will compile a list of consumer
organizations that will participate in the selection process and will
forward to each such organization a ballot listing three to five
qualified nominees selected by the Agency based on the nominations
received, together with each nominee's current curriculum vitae or
resume. Ballots are to be filled out and returned to FDA within 30
days. The nominee receiving the highest number of votes ordinarily will
be selected to serve as the member representing consumer interests for
that particular advisory committee or panel.

IV. Nomination Procedures

    Any interested person or organization may nominate one or more
qualified persons to represent consumer interests on the Agency's
advisory committees or panels. Self-nominations are also accepted.
Potential candidates will be required to provide detailed information
concerning such matters as financial holdings, employment, and research
grants and/or contracts to permit evaluation of possible sources of
conflicts of interest.
    All nominations should include: a cover letter; a curriculum vitae
or resume that includes the nominee's office address, telephone number,
and email address; and a list of consumer or community-based
organizations for which the candidate can demonstrate active
participation.
    Nominations also should specify the advisory committee(s) or
panel(s) for which the nominee is recommended. In addition, nominations
should include confirmation that the nominee is aware of the nomination
and is willing to serve as a member of the advisory committee or panel
if selected.
    The term of office is up to 4 years. FDA will review all
nominations received within the specified timeframes and prepare a
ballot containing the names of qualified nominees. Names not selected
will remain on a list of eligible nominees and be reviewed periodically
by FDA to determine continued interest. Upon selecting qualified
nominees for the ballot, FDA will provide those consumer organizations
that are participating in the selection process with the opportunity to
vote on the listed nominees. Only organizations vote in the selection
process. Persons who nominate themselves to serve as voting or
nonvoting consumer representatives will not participate in the
selection process.
    FDA seeks to include the views of women and men, members of all
racial and ethnic groups, and individuals with and without disabilities
on its advisory committees and therefore, encourages nominations of
appropriately qualified candidates from these groups.
    This notice is issued under the Federal Advisory Committee Act (5
U.S.C. app. 2) and 21 CFR part 14 relating to advisory committees.

    Dated: February 15, 2013.
Jill Hartzler Warner,
Acting Associate Commissioner for Special Medical Programs.
[FR Doc. 2013-04059 Filed 2-21-13; 8:45 am]
BILLING CODE 4160-01-P