1

HAP benefits

Due to data, resource, and methodology limitations, we were unable to estimate the 

benefits associated with the 1,014 tons of hazardous air pollutants that would be reduced as a 

result of this rule. Available emissions data show that several different HAPs are emitted from 

stationary engines, either contained within the fuel burned or formed during the combustion 

process. The HAPs measured in emission tests conducted on diesel fired stationary RICE 

include 1,3-butadiene, acetaldehyde, acrolein, benzene, ethylbenzene, formaldehyde, n-hexane, 

naphthalene, polycyclic aromatic hydrocarbons (PAHs), polycyclic organic matter, styrene, 

toluene, and xylene. Metallic HAPs from diesel fired stationary RICE that have been measured 

include cadmium, chromium, lead, manganese, mercury, nickel, and selenium.

Although numerous HAPs may be emitted from RICE, a few HAPs account for 80% of 

the total mass of HAPs emissions from diesel stationary RICE. These HAPs are formaldehyde 

(25%), acetaldehyde (19%), PAH (18%), naphthalene (9%), and acrolein (9%).

Formaldehyde

Since 1987, EPA has classified formaldehyde as a probable human carcinogen based on 

evidence in humans and in rats, mice, hamsters, and monkeys.1 EPA is currently reviewing 

recently published epidemiological data. For instance, research conducted by the National 

Cancer Institute (NCI) found an increased risk of nasopharyngeal cancer and 

lymphohematopoietic malignancies such as leukemia among workers exposed to 

formaldehyde.2,3 In an analysis of the lymphohematopoietic cancer mortality from an extended 

follow-up of these workers, NCI confirmed an association between lymphohematopoietic cancer 

risk and peak exposures.4 A recent National Institute of Occupational Safety and Health 

(NIOSH) study of garment workers also found increased risk of death due to leukemia among 

workers exposed to formaldehyde.5

 

Formatted: Highlight

1 U.S. EPA. 1987. Assessment of Health Risks to Garment Workers and Certain Home Residents from Exposure to 

Formaldehyde, Office of Pesticides and Toxic Substances, April 1987.

 Extended follow-up of a cohort of British chemical workers 

2 Hauptmann, M..; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.; Blair, A. 2003. Mortality from lymphohematopoetic 

malignancies among workers in formaldehyde industries. Journal of the National Cancer Institute 95: 1615-

1623. 3 Hauptmann, M..; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.; Blair, A. 2004. Mortality from solid cancers among 

workers in formaldehyde industries. American Journal of Epidemiology 159: 1117-1130. 4 Beane Freeman, L. E.; Blair, A.; Lubin, J. H.; Stewart, P. A.; Hayes, R. B.; Hoover, R. N.; Hauptmann, M. 2009. 

Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries: The National 

Cancer Institute cohort. J. National Cancer Inst. 101: 751-761. 5 Pinkerton, L. E. 2004. Mortality among a cohort of garment workers exposed to formaldehyde: an update. Occup. 

Environ. Med. 61: 193-200.

Comment [A1]: This is a list of 13 

compounds. However just below, in 

highlight, 5 compounds are emphasized. 

What are the % mass releases of these 

other 8? It would make sense for EPA to 

list and discuss them in order of most to 

least. Its not clear that many of them are 

released . We note that the write up below 

discusses 5 compounds one of these is 

not listed in highlight( POM) This is very 

confusing. We suggest a write up that 

includes the 5 in highlight. Unclear why 

the total list of 13 is provided without any 

context.
2

did not find evidence of an increase in nasopharyngeal or lymphohematopoietic cancers, but a 

continuing statistically significant excess in lung cancers was reported.6

In the past 15 years there has been substantial research on the inhalation dosimetry for 

formaldehyde in rodents and primates by the CIIT Centers for Health Research (formerly the 

Chemical Industry Institute of Toxicology), with a focus on use of rodent data for refinement of 

the quantitative cancer dose-response assessment.7,8,9 CIIT’s risk assessment of formaldehyde 

incorporated mechanistic and dosimetric information on formaldehyde. However, it should be 

noted that recentRecent research published by EPA indicates that when two-stage modeling 

assumptions are varied, resulting dose-response estimates can vary by several orders of 

magnitude.10,11,12,13 These findings are not supportive of interpreting the CIIT model results as 

providing a conservative (health protective) estimate of human risk.14 EPA research also 

examined the contribution of the two-stage modeling for formaldehyde towards characterizing 

the relative weights of key events in the mode-of-action of a carcinogen. For example, in one 

particular paper, the model-based inference in the published CIIT study that formaldehyde’s 

direct mutagenic action is not relevant to the compound’s tumorigenicity was found not to hold 

under variations of modeling assumptions.15

 6 Coggon, D, EC Harris, J Poole, KT Palmer. 2003. Extended follow-up of a cohort of British chemical workers 

exposed to formaldehyde. J National Cancer Inst. 95:1608-1615. 7Conolly, RB, JS Kimbell, D Janszen, PM Schlosser, D Kalisak, J Preston, and FJ Miller. 2003. 

Biologically motivated computational modeling of formaldehyde carcinogenicity in the F344 

rat. Tox Sci 75: 432-447. 8Conolly, RB, JS Kimbell, D Janszen, PM Schlosser, D Kalisak, J Preston, and FJ Miller. 2004. 

Human respiratory tract cancer risks of inhaled formaldehyde: Dose-response predictions 

derived from biologically-motivated computational modeling of a combined rodent and 

human dataset. Tox Sci 82: 279-296. 9Chemical Industry Institute of Toxicology (CIIT).1999. Formaldehyde: Hazard characterization 

and dose-response assessment for carcinogenicity by the route of inhalation. CIIT, September 

28, 1999. Research Triangle Park, NC. 10 U.S. EPA. Analysis of the Sensitivity and Uncertainty in 2-Stage Clonal Growth Models for Formaldehyde with 

Relevance to Other Biologically-Based Dose Response (BBDR) Models. U.S. Environmental Protection Agency, 

Washington, D.C., EPA/600/R-08/103, 2008 11 Subramaniam, R; Chen, C; Crump, K; .et .al. (2008) Uncertainties in biologically-based modeling of 

formaldehyde-induced cancer risk: identification of key issues. Risk Anal 28(4):907-923. 12 Subramaniam, R; Chen, C; Crump, K; .et .al. (2007). Uncertainties in the CIIT 2-stage model for formaldehydeinduced nasal cancer in the F344 rat: a limited sensitivity analysis-I. Risk Anal 27:1237 13 Crump, K; Chen, C; Fox, J; .et .al. (2008) Sensitivity analysis of biologically motivated model for formaldehydeinduced respiratory cancer in humans. Ann Occup Hyg 52:481-495. 14 Crump, K; Chen, C; Fox, J; .et .al. (2008) Sensitivity analysis of biologically motivated model for formaldehydeinduced respiratory cancer in humans. Ann Occup Hyg 52:481-495. 15 Subramaniam, R; Chen, C; Crump, K; .et .al. (2007). Uncertainties in the CIIT 2-stage model for formaldehydeinduced nasal cancer in the F344 rat: a limited sensitivity analysis-I. Risk Anal 27:1237

Comment [A2]: Edit made for tone. We 

note that all this information seems to get 

into a he said/she said type discussion 

which really seems inappropriate. EPA 

should simply say a new IRIS assessment 

will be forthcoming after review of all the 

science and not get into picking certain 

new studies to cite and certain new studies 

to dis-credit.

Comment [A3]: Unclear exactly what 

this means. Do you mean protection of 

sensitive subpopulations? Preference 

would be to delete this as being an 

unnecessary interpretation but alternative 

approach would be to use a direct quote 

from the authors of the paper. Perhaps 

EPA should use these sentences from the 

paper: “However, the analysis presented 

herein shows that the Conolly et al. model 

is highly sensitive to uncertain model 

assumptions, and other reasonable 

assumptions are equally compatible with

the data but lead to much higher risks. 

These risks can be considerably higher 

than what would be obtained using 

standard statistical modeling approaches 

(USEPA, 2005). Thus, the formaldehyde 

humanmodel cannot reasonably be used 

to narrow the range of low-dose human 

risk over that predicted by the standard 

regulatory approach.” (in the discussion). 

The abstract has the following conclusion, 

but the context would need explaining for 

use here: “Thus, we conclude that 

estimates of human risk by Conolly et al.

(2004) are extremely sensitive to 

modeling assumptions. This calls into 

question the basis for the Conolly et al.

claim of de minimis human risk and 

suggests caution in using the model to 

derive human exposure standards for 

formaldehyde.”

Comment [A4]: Need citation
3

Based on the developments of the last decade, in 2004, the working group of the IARC 

concluded that formaldehyde is carcinogenic to humans (Group 1), on the basis of sufficient 

evidence in humans and sufficient evidence in experimental animals - a higher classification than 

previous IARC evaluations. After reviewing the currently available epidemiological evidence, 

the IARC (2006) characterized the human evidence for formaldehyde carcinogenicity as 

“sufficient,” based upon the data on nasopharyngeal cancers; the epidemiologic evidence on 

leukemia was characterized as “strong.”16

Formaldehyde exposure also causes a range of noncancer health effects, including 

irritation of the eyes (burning and watering of the eyes), nose and throat. Effects from repeated 

exposure in humans include respiratory tract irritation, chronic bronchitis and nasal epithelial 

lesions such as metaplasia and loss of cilia. Animal studies suggest that formaldehyde may also 

cause airway inflammation – including eosinophil infiltration into the airways. There are several 

studies that suggest that formaldehyde may increase the risk of asthma – particularly in the 

young.

EPA is reviewing the recent work cited above from 

the NCI and NIOSH, as well as the analysis by the CIIT Centers for Health Research and other 

studies, as part of a reassessment of the human hazard and dose-response associated with 

formaldehyde.

17,18

Acetaldehyde is classified in EPA’s IRIS database as a probable human carcinogen, 

based on nasal tumors in rats, and is considered toxic by the inhalation, oral, and intravenous 

routes.

 Acetaldehyde

19

 16 International Agency for Research on Cancer (2006) Formaldehyde, 2-Butoxyethanol and 1-tert-Butoxypropan-2-

ol. Monographs Volume 88. World Health Organization, Lyon, France.

 Acetaldehyde is reasonably anticipated to be a human carcinogen by the U.S. DHHS in 

the 11th Report on Carcinogens and is classified as possibly carcinogenic to humans (Group 2B) 

17 Agency for Toxic Substances and Disease Registry (ATSDR). 1999. Toxicological profile for Formaldehyde. 

Atlanta, GA: U.S. Department of Health and Human Services, Public Health Service. 

http://www.atsdr.cdc.gov/toxprofiles/tp111.html

18 WHO (2002) Concise International Chemical Assessment Document 40: Formaldehyde. Published under the 

joint sponsorship of the United Nations Environment Programme, the International Labour Organization, and the 

World Health Organization, and produced within the framework of the Inter-Organization Programme for the 

Sound Management of Chemicals. Geneva. 19 U.S. EPA (1988). Integrated Risk Information System File of Acetaldehyde. Research and Development, 

National Center for Environmental Assessment, Washington, DC. This material is available electronically at 

http://www.epa.gov/iris/subst/0290.htm.

Comment [A5]: Please provide IARC 

citation.

Comment [A6]: Please provide citation 

for all of the sentences in this paragraph..
4

by the IARC.20,21

The primary noncancer effects of exposure to acetaldehyde vapors include irritation of 

the eyes, skin, and respiratory tract.

 EPA is currently conducting a reassessment of cancer risk from inhalation 

exposure to acetaldehyde.

22 In short-term (4 week) rat studies, degeneration of 

olfactory epithelium was observed at various concentration levels of acetaldehyde exposure.23,24 

Data from these studies were used by EPA to develop an inhalation reference concentration. 

Some asthmatics have been shown to be a sensitive subpopulation to decrements in functional 

expiratory volume (FEV1 test) and bronchoconstriction upon acetaldehyde inhalation.25 The 

agency is currently conducting a reassessment of the health hazards from inhalation exposure to 

acetaldehyde. 

POM is generally defined as a large class of organic compounds which have multiple 

benzene rings and a boiling point greater than 100 degrees Celsius. Many of the compounds 

included in the class of compounds known as POM are classified by EPA as probable human 

carcinogens based on animal data. One of these compounds, naphthalene, is discussed separately 

below. Polycyclic aromatic hydrocarbons (PAHs) are a subset of POM that contain only 

hydrogen and carbon atoms. A number of PAHs are known or suspected carcinogens. EPA’s 

IRIS program has not evaluated the health effects of PAH’s, although ATSDR has conducted a 

review of non-cancer effects.Recent studies have found that maternal exposures to PAHs (a 

subclass of POM) in a population of pregnant women were associated with several adverse birth 

outcomes, including low birth weight and reduced length at birth, as well as impaired cognitive 

development at age three.

Polycyclic Organic Matter (POM)Polyaromatic Hydrocarbons

26,27

 20 U.S. Department of Health and Human Services National Toxicology Program 11th Report on Carcinogens 

available at: http://ntp.niehs.nih.gov/go/16183.

 EPA has not yet evaluated these recent studies. PAHs can be 

21 International Agency for Research on Cancer (IARC). 1999. Re-evaluation of some organic chemicals, hydrazine, 

and hydrogen peroxide. IARC Monographs on the Evaluation of Carcinogenic Risk of Chemical to Humans, 

Vol 71. Lyon, France. 22 U.S. EPA (1988). Integrated Risk Information System File of Acetaldehyde. This material is available 

electronically at http://www.epa.gov/iris/subst/0290.htm. 23 U.S. EPA. 2003. Integrated Risk Information System File of Acrolein. Research and Development, National 

Center for Environmental Assessment, Washington, DC. This material is available electronically at 

http://www.epa.gov/iris/subst/0364.htm. 24 Appleman, L.M., R.A. Woutersen, and V.J. Feron. (1982). Inhalation toxicity of acetaldehyde in rats. I. Acute and 

subacute studies. Toxicology. 23: 293-297. 25 Myou, S.; Fujimura, M.; Nishi K.; Ohka, T.; and Matsuda, T. (1993) Aerosolized acetaldehyde induces 

histamine-mediated bronchoconstriction in asthmatics. Am. Rev. Respir.Dis.148(4 Pt 1): 940-943. 26 Perera, F.P.; Rauh, V.; Tsai, W-Y.; et al. (2002) Effect of transplacental exposure to environmental pollutants on 

birth outcomes in a multiethnic population. Environ Health Perspect. 111: 201-205.

Comment [A7]: This section should be 

replaced with a discussion that focuses on 

PAH’s only (like is done for naphthalene)

Comment [A8]: Provide citation—

perhaps this is NTP?
5

harmful to your health under some circumstances. Several of the PAHs, including 

benz[a]anthracene, benzo[a]pyrene, benzo[b]fluoranthene, benzo[j]fluoranthene, 

benzo[k]fluoranthene, chrysene, dibenz[a,h]anthracene, and indeno[1,2,3-c,d]pyrene, have 

caused tumors in laboratory animals when they breathed these substances in the air, when they 

ate them, or when they had long periods of skin contact with them. Studies of people show that 

individuals exposed by breathing or skin contact for long periods to mixtures that contain PAHs 

and other compounds can also develop cancer. 28

Naphthalene is found in small quantities in gasoline and diesel fuels. Naphthalene 

emissions have been measured in larger quantities in both gasoline and diesel exhaust compared 

with evaporative emissions from mobile sources, indicating it is primarily a product of 

combustion. EPA, in 2004, released an external review draft of a reassessment of the inhalation 

carcinogenicity of naphthalene based on a number of recent animal carcinogenicity studies.

Naphthalene

29 

The draft reassessment completed external peer review.30 Based on external peer review 

comments received, additional analyses are being undertaken. This external review draft does 

not represent official agency opinion and was released solely for the purposes of external peer 

review and public comment. The National Toxicology Program listed naphthalene as 

"reasonably anticipated to be a human carcinogen" in 2004 on the basis of bioassays reporting 

clear evidence of carcinogenicity in rats and some evidence of carcinogenicity in mice.31 

California EPA has released a new risk assessment for naphthalene, and the IARC has 

reevaluated naphthalene and re-classified it as Group 2B: possibly carcinogenic to humans.32

 27 Perera, F.P.; Rauh, V.; Whyatt, R.M.; Tsai, W.Y.; Tang, D.; Diaz, D.; Hoepner, L.; Barr, D.; Tu, Y.H.; Camann, 

D.; Kinney, P. (2006) Effect of prenatal exposure to airborne polycyclic aromatic hydrocarbons on 

neurodevelopment in the first 3 years of life among inner-city children. Environ Health Perspect 114: 1287-

1292.

 

28 http://www.atsdr.cdc.gov/toxprofiles/phs69.html 29 U. S. EPA. 2004. Toxicological Review of Naphthalene (Reassessment of the Inhalation Cancer Risk), 

Environmental Protection Agency, Integrated Risk Information System, Research and Development, National 

Center for Environmental Assessment, Washington, DC. This material is available electronically at 

http://www.epa.gov/iris/subst/0436.htm. 30 Oak Ridge Institute for Science and Education. (2004). External Peer Review for the IRIS Reassessment of the 

Inhalation Carcinogenicity of Naphthalene. August 2004. 

http://cfpub.epa.gov/ncea/cfm/recordisplay.cfm?deid=84403 31 National Toxicology Program (NTP). (2004). 11th Report on Carcinogens. Public Health 

Service, U.S. Department of Health and Human Services, Research Triangle Park, NC. 

Available from: http://ntp-server.niehs.nih.gov. 32 International Agency for Research on Cancer (IARC). (2002). Monographs on the Evaluation 

of the Carcinogenic Risk of Chemicals for Humans. Vol. 82. Lyon, France.
6

Naphthalene also causes a number of chronic non-cancer effects in animals, including abnormal 

cell changes and growth in respiratory and nasal tissues.33

EPA determined in 2003 that the human carcinogenic potential of acrolein could not be 

determined because the available data were inadequate. No information was available on the 

carcinogenic effects of acrolein in humans and the animal data provided inadequate evidence of 

carcinogenicity.

 Acrolein

34 The IARC determined in 1995 that acrolein was not classifiable as to its 

carcinogenicity in humans.

35

Acrolein is extremely acrid and irritating to humans when inhaled, with acute exposure 

resulting in upper respiratory tract irritation, mucus hypersecretion and congestion. The intense 

irritancy of this carbonyl has been demonstrated, in 1957, during controlled tests in human 

subjects, who suffer intolerable eye and nasal mucosal sensory reactions within minutes of 

exposure.36 These data and additional studies which are more recent and more reliable for 

determining safe exposure levels, regarding acute effects of human exposure to acrolein are 

summarized in EPA’s 2003 IRIS Human Health Assessment for acrolein.37 Evidence available 

from studies in humans indicate that levels as low as 0.09 ppm (0.21 mg/m3) for five minutes 

may elicit subjective complaints of eye irritation with increasing concentrations leading to more 

extensive eye, nose and respiratory symptoms.38 Lesions to the lungs and upper respiratory tract 

of rats, rabbits, and hamsters have been observed after subchronic exposure to acrolein.39 Acute 

exposure effects in animal studies report bronchial hyper-responsiveness.40

 33 U. S. EPA. 1998. Toxicological Review of Naphthalene, Environmental Protection Agency, Integrated Risk 

Information System, Research and Development, National Center for Environmental Assessment, Washington, 

DC. This material is available electronically at http://www.epa.gov/iris/subst/0436.htm

 In a recent study, the 

34 Integrated Risk Information System File of Acrolein. Research and Development, National Center for 

Environmental Assessment, Washington, DC. This material is available at http://www.epa.gov/iris/subst/0364.htm 35 International Agency for Research on Cancer (IARC). 1995. Monographs on the evaluation of 

carcinogenic risk of chemicals to humans, Volume 63, Dry cleaning, some chlorinated 

solvents and other industrial chemicals, World Health Organization, Lyon, France. 36 Sim VM, Pattle RE. Effect of possible smog irritants on human subjects JAMA165: 1980-2010, 1957. 37 U.S. EPA (U.S. Environmental Protection Agency). (2003) Toxicological review of acrolein in support of 

summary information on Integrated Risk Information System (IRIS) National Center for Environmental 

Assessment, Washington, DC. EPA/635/R-03/003. Available online at: http://www.epa.gov/ncea/iris. 38 Weber-Tschopp, A; Fischer, T; Gierer, R; et al. (1977) Experimentelle reizwirkungen von Acrolein auf den 

Menschen. Int Arch Occup Environ Hlth 40(2):117-130. In German 39 Integrated Risk Information System File of Acrolein. Office of Research and Development, National Center for 

Environmental Assessment, Washington, DC. This material is available at http://www.epa.gov/iris/subst/0364.htm 40 U.S. EPA (U.S. Environmental Protection Agency). (2003) Toxicological review of acrolein in support of summary 

information on Integrated Risk Information System (IRIS) National Center for Environmental Assessment, 

Washington, DC. EPA/635/R-03/003. Available online at: http://www.epa.gov/ncea/iris.

Comment [A10]: Suggest deletion and 

replacing with the study in English upon 

which the IRIS RfC is based. This is more 

relevant
7

acute respiratory irritant effects of exposure to 1.1 ppm acrolein were more pronounced in mice 

with allergic airway disease by comparison to non-diseased mice which also showed decreases in 

respiratory rate.41 Based on these animal data and demonstration of similar effects in humans 

(i.e., reduction in respiratory rate), EPA expects that individuals with compromised respiratory 

function (e.g., emphysema, asthma) are expected to bmay be ate at increased risk of developing 

adverse responses to strong respiratory irritants such as acrolein. 

In addition to the compounds described above, other compounds in gaseous hydrocarbon 

and PM emissions from RICE engines would be affected by this rule. Information regarding the 

health effects of these compounds can be found in EPA’s IRIS database.

Other Air Toxics

42

The distance that these HAPs travel away from the emission source depends on several 

factors. HAPs such as formaldehyde, acetaldehyde, PAHs, and acrolein are emitted as gases. 

Regional photochemical model simulations have shown that gaseous HAPs like formaldehyde 

and acetaldehyde can be transported hundreds of kilometers from their emissions source in 

distinct plumes (U.S. EPA, 2010b). Further, these emissions can contribute to regional airmasses 

with elevated concentrations of gaseous HAPs. These polluted airmasses can be transported 

thousands of kilometers and affect locations well distant from the original emissions source. 

Some gaseous HAPs transform into particles in the atmosphere. For HAPs emitted as particles, 

such as metals, the travel distance primarily depends on the size of the particle and 

meteorological conditions, such as wind speed and precipitation. Fine particles can have an 

atmospheric half-life of days to weeks and travel hundreds to thousands of kilometers, whereas 

ultrafine and coarse particles travel less than ten kilometers (U.S. EPA, 2009c). 

Carbon monoxide co-benefits

Carbon monoxide (CO) exposure is associated with a variety of health effects. Without 

knowing the location of the emission reductions and the resulting ambient concentrations using 

fine-scale air quality modeling, we were unable to estimate the exposure to CO for nearby 

populations. Due to data limitations, we were unable to estimate the benefits associated with the 

14,000 tons reductions in CO emissions that would occur as a result of this rule. 

 41 Morris JB, Symanowicz PT, Olsen JE, et al. 2003. Immediate sensory nerve-mediated respiratory responses to 

irritants in healthy and allergic airway-diseased mice. J Appl Physiol 94(4):1563-1571. 42 U.S. EPA Integrated Risk Information System (IRIS) database is available at: www.epa.gov/iris

Comment [A11]: Caveat needed here as 

it is well known that animal models are 

not good surrogates for humans with 

emphysema or asthma thus this statement 

seems a bit odd and since no direct 

science supports it, need to be clear that 

this is an EPA inference.

Comment [A12]: What is this. If it is a 

TSD has it been peer reviewed? If not, 

please mention this and discuss plans for 

reviewing the modeling results. Because it 

is a TSD for a rule, does not automatically 

mean that it meets IQ standards and 

should be relied upon as scientifically 

correct in its conclusions. Peer review is 

important.

Comment [A13]: Which ones? What 

percentile? What determines if this 

happens? Without knowing this then 

essentially we know nothing about how 

far a hap like formaldehyde or 

acetaldehyde will travel.

Comment [A14]: See comment above 

regarding peer review. This sentence 

seems very generic. If the bottom line is 

that we know nothing about how HAPs 

from RICE will travel, we should say that 

more clearly.