Call for Comments and Testimony
 EPA Administrator Defies Science, Law, Staff and Advisors: 

Proposes to Keep National Ambient Air Quality Standards 
for Carbon Monoxide at 1971 Levels

 7 critical problems with EPA’s CO rulemaking identified by Albert Donnay, MHS, adonnay@jhu.edu
Consulting Toxicologist, Environmental Health Engineer and Certified Carbon Monoxide Analyst

1. EPA Administrator Lisa Jackson rejects recommendations of both EPA staff and EPA’s Clean Air Scientific Advisory Committee to consider lowering CO standards from 9parts per million (ppm) to as low as 3-4ppm for the maximum 8-hour average exposure, and from 35ppm to as low as 5-8ppm for maximum average-1 hour exposure, 

despite over 100 epidemiology studies published since 1979 showing significant increases in the risk of morbidity and mortality from both cardiovascular and respiratory diseases as well as even higher risks of low birth weight, birth defects and neonatal mortality--and all from small increases in CO (most just 0.1-1ppm) within the range of current CO exposures.  Note 8-hour avg. CO levels have been under 9ppm since 1991 and are now below 3 with a mean of just 2 (white line below, source = EPA

2. EPA’s Integrated Science Assessment of CO, upon which EPA’s CO standard is supposed to be based, reviews only 817 documents of any kind, including just 455 in the chapter on CO “Integrated Health Effects,”

 despite over 24,000 peer-reviewed articles mentioning CO available from www.pubmed.gov, approximately 5,000 which are included in the bibliography that EPA compiled for its CO NAAQS assessment (searchable at http://hero.epa.gov).   Since EPA completed its last review of the CO standard in 1994, the number of CO-related articles has more than doubled.  While EPA’s HERO file contains 52% of those published from 1994 to 2000, it contains only 9% of the more than 8,000 published since.  EPA’s CO rulemaking process ignored 91% of the peer-reviewed CO literature published in the last decade.

3. EPA Administrator claims the “uncertainties and limitations” of the available epidemiological data are “too great for the epidemiological evidence to provide a basis for revising the current standards,”

despite EPA relying on many of the same multi-pollutant studies as the basis for proposed reductions in NAAQS standards for particulate matter, nitrous oxide, sulfur dioxide and ozone, including studies in which the relative risk associated with each interquartile range increase in ambient CO exposure (usually <1ppm), or from lowest to highest exposure (usually less than 5ppm) is greater than that for any other pollutant.  EPA’s Integrated Science Assessment also includes only epi studies of cardiovascular disorders (mainly stroke, congestive heart failure, MI and ECG abnormalities), respiratory disorders (allergy, asthma, COPD), and birth outcomes (preterm birth, low birth weight, heart defects and neonatal mortality).  While these are all significantly associated with small interquartile range increases in outdoor CO of less than 2ppm and most less than 1ppm, so are many other conditions not mentioned in EPA’s CO ISA, its CO Risk and Exposure Assessment, its CO Policy Assessment, or its Proposed Rulej,.  These include ear infections and gastroenteric illness in children, and ER visits and/or hospitalizations in adults for appendicitis, depression, epilepsy, headache and pneumonia (also pneumonia mortality).

4.  EPA Administrator endorses keeping exclusive focus on carboxyhemoglobin (COHb) as “metric of concern,” with goal of keeping COHb under 2% to protect people with cardiovascular disease from developing angina (which small controlled exposure studies from the 1970s and 1980s found starting at 2% COHb after exposure to over 100ppm),

despite decades of literature documenting that COHb does not correlate consistently with the symptoms, severity or outcome of CO poisoning, especially in the range of ambient CO exposures (under 5ppm) which do not raise COHb even 1%.  Even the WHO has recognized since 2000 that “ambient CO may have even more serious health consequences than does COHb formation and at lower levels than that mediated through elevated COHb levels” and that there is “no threshold for the onset of these effects.”  This is because many effects of CO are not caused by hypoxia from CO binding to hemoglobin in blood but from unbound CO diffusing (like oxygen) through plasma into muscles, brain and other organs where it binds to myoglobin, neuroglobin, cytochromes and other intracellular heme proteins (see ATSDR's draft Tox Profile on CO for more on CO activity in tissues and organs that is unrelated to COHb) 

Epi studies also show the increased risk of angina pectoris hospitalizations (<1% per 1ppm of CO) is much less than for stroke mortality (8.3% per 0.1ppm), asthma hospitalization (16% per 1ppm), neonatal (2-3mo) respiratory mortality (36% per 1ppm) and, unassociated with any other pollutants, cardiac ventricular septal birth defects (with Odds Ratios increasing in  dose response fashion from 1.62 above 1.14ppm, 2.09 above 1.57ppm and 2.95 above 2.39ppm).

5.  EPA Administrator ignores all studies that used the level of exhaled CO in breath as a measure of exposure,

despite over 1,000 articles documenting that exhaled CO is a more sensitive and relevant biomarker of CO body burden than COHb.  This metric is also much more useful than COHb when considering epi studies, since breath CO, like CO exposure, is measured in ppm.  This allows direct comparison of ambient CO levels with endogenous CO levels produced from metabolism of heme proteins.  Breath CO is normally just 0-2ppm but is higher with recent or chronic CO exposure and also predicts risk of developing metabolic syndrome (OR=1.48) and first cardiovascular event (HR=1.66).

6.  EPA Administrator only recognizes the significance of low level CO exposures to people with cardiovascular disorders and does not mention the association of CO with asthma,

despite an entire section devoted to asthma in EPA’s Integrated Science Assessment on CO which concludes: “Specifically, among asthmatics, the studies reviewed generally found positive associations between short-term exposure to CO and respiratory-related health effects (i.e. decrements in lung function, respiratory symptoms, and medication use” (p.5-88).  Yet there is no mention of these findings in EPA’s Risk and Exposure Assessment for CO--where the word asthma only appears twice--or in EPA’s Policy Assessment for the CO Review, or its Proposed Rule, where the word asthma does not even appear.  Instead, whenever these other EPA documents acknowledge pre-existing diseases of concern other than cardiovascular conditions “that may have already limited oxygen availability or increased COHb production,” they list only “obstructive lung diseases, diabetes and anemia.”  Although both fetuses and the elderly are also both correctly identified in EPA’s ISA as “susceptible populations,” asthmatics are not.   Despite over 300 studies in the last 30 years documenting the role of CO in asthma, EPA’s publications and webpages on CO do not mention asthma and none on asthma mention CO.

7.  EPA Administrator and staff claim there is only “preliminary evidence” of “a mechanism that could provide plausibility for CO-induced effects” seen in epidemiological studies at low levels of exposure, and that these effects are more likely due either to a mix of other traffic pollutants or to other as yet unidentified pollutants,

        despite many studies on endogenous CO reviewed in EPA’s ISA--and many more not reviewed--that document  
a) many non-COHb and non-hypoxic pathways by which CO is involved in the etiology of respiratory, neurological, and cardiovascular disorders (see 2000 review by a CO expert working with EPA as a visiting scientist);
b) significant increased risks of various adverse outcomes associated with 0.1-1ppm increases in ambient CO that persist even in multi-pollutant analyses adjusted for the interactive effects PM, SO2, NO2 and O3; and
c) recognition by the US Agency for Toxic Substances and Disease Registry in its draft Tox Profile on CO that, “given the physiological role of endogenous CO…, any exogenous source of carbon monoxide exposure” has “the potential for producing potentially adverse effects” (p20). 

CRITICAL ACTION REQUESTED:  All those who submitted comments in support of reducing EPA’s NAAQS for NO2, SO2, PM or ozone are encouraged to do so for CO as well.  The same susceptible populations are even more at risk from CO and will remain so until CO exposures are lowered.  Given that CO epidemiology studies have found increased adverse affects from 8-hour average CO levels in the range of 1-2ppm , even the lowest standard recommended by EPA staff of 3-4ppm is not low enough to protect public health.   The new 8-hour standard should be no more than 1ppm, and the 1-hour standard no more than the 5ppm minimum suggested by EPA staff.  Those unable to submit their own comments are invited to sign a petition to EPA in favor of lower CO standards.  For more information, please contact Albert Donnay.

    * All EPA CO NAAQS documents are available online at www.epa.gov/ttn/naaqs/standards/co/s_co_index.html

    * SEND PUBLIC COMMENTS by 4/12/2011 to a-and-r-Docket@epa.gov  and specify Docket # EPA-HQ-OAR-2008-0015

    * PUBLIC HEARING is 2/28/2011 at EPA office in Arlington VA. To pre-register, call or email Jan King at 919-541-5665