Comments on draft Ch. 5 of the RIA for PM (August 16, 2006)

The brief comments on draft Ch. 5 have to do with the issues of
uncertainty and of differential toxicity brought up in the draft
chapter.  

Summary

The draft RIA, Ch. 5, should discuss specific sensitivities in at least
some detail, rather than briefly mentioning them (sometimes with
ambiguous wording).  If sensitivities are to be brought up (as we agree
they should be), then some important ones not presently identified
and/or discussed should be identified and discussed.

Discussion

A.  In the last paragraph on pg. 5-23 is the following passage:

“While the HEI reexamination lends credibility to the original
studies, it also highlights sensitivities concerning the relative impact
of various pollutants, the potential role of education in mediating the
association between pollution and mortality, and the influence of
spatial correlation modeling.  Further confirmation and extension of the
overall findings using more recent air quality and a longer follow-up
period for the ACS cohort was recently published (Pope et al., 2002  XE
"Pope et al., 2002"  )….”

The draft is correct to highlight sensitivities, but it fails to note
important sensitivities, some of which were spelled out in the Preamble
of Jan. 17.  Among these are:

1.  The influence of spatial correlation modeling appears to refer to
the fact that when the gas SO2 is included in the model of Krewski et al
(2000), the fine PM and the sulfate risk coefficients are sharply
reduced and become insignificant, while the SO2 risk coefficient remains
large and significant.  Commenters have suggested that the dominance of
SO2 may be reflective that PM emissions from specific local sources of
SO2 (such as steel mills and coke ovens of the time period of these
studies, starting in the early 1980s) were the most health-relevant.

The January 17 Preamble discusses this issue on pp. 2652/3.  It points
out that the Pope et al (2002) follow-up analysis failed to include
multi-pollutant modeling, in particular with regard to SO2.  

Thus the discussion on pg. 5-23 could be augmented by explaining more
fully what is meant by the ambiguous passage “and the influence of
spatial correlation modeling” and by pointing out that the Pope et al
(2002) follow-up skirted the issue.  If this ambiguous passage does NOT
refer to the SO2/multipollutant modeling issue, then it should include
discussion of this issue.

2.  Neither the ACS study nor the Six Cities study monitored for health
relevant local pollutants such as PAHs and BC/EC, metals such as Ni and
V, and proxies for specific source exposure such as vehicle miles
traveled per square mile.  While central monitor studies have
methodological infirmities that have been improved upon by more recent
studies using more sophisticated methodologies, nevertheless monitoring
for emissions and proxides such as these could have pointed to specific
sources and might have driven fine PM to statistical insignificance, as
inclusion of SO2 has already done.

Thus in a discussion of sensitivities of the ACS and Six Cities studies,
and of the Krewski et al (2000) reanalysis, the sensitivity of the many
pollutant and proxies not monitored is important, and should be
mentioned here.

Finally, two additional recent publications discuss in detail these
issues of sensitivity, and therefore, along with Krewski et al (2000)
should also be referenced and discussed: these are Jerrett et al (2003)
and Jerrett and Finkelstein (2005).

B.  On pg. 5-35, there is a discussion of Uncertainties in the PM
Mortality Relationship.  The discussion of Other Pollutants is very
short and uninformative, and should be expanded substantially.  

For example, there are three cohort studies (from 2002, 2004, and 2005)
showing that those who live in close proximity to highways and major
urban roads have highly elevated risks of mortality and cardiovascular
morbidity, far higher than in Pope et al (2002), the ACS follow-up. 
Highway emissions include VOCs and SVOCs which are highly correlated
with vehicular PM; in fact, the mass of just SVOCs from a clean burning
diesel engine is greater than the mass of PM from the engine.  PAHs come
in all three physical forms (VOC, SVOC, and PM), with PM PAHs often in
the ultrafine size mode.

Toxicology as well shows that emissions from such roads have substantial
health effects (McDonald et al, 2004; Seagrave et al, 2006).  DOE’s
May 1 comments included a 47 page section discussing the many studies
(epidemiology, CAPs, and toxicology) suggesting many different health
effects attributable to vehicular emissions.

So one uncertainty, with regard to Other Pollutants, would be emissions
from highway vehicles, and this uncertainty should be specifically noted
and briefly discussed.

Other Pollutants should also briefly identify residual fuel fly ash
(ROFA) and Ni as also being pollutants with identifiable specific
effects, based upon a number of recent studies.

C. On pg. 5-36, there is a discussion of relative toxicity, including
this passage:

However, to provide information that may be useful as additional studies
become available, we are providing estimates of the proportions of
benefits that are attributable to specific components of PM2.5, e.g.,
ammonium sulfate, ammonium nitrate, elemental carbon, organic carbon,
and crustal material (which includes metals).

1.  Where is this information provided?  

2.  Are there going to be sensitivity analyses, based upon assumptions
of differential toxicities of different types of fine PM?

3.  As a recommendation – recognizing that EPA does not at this point
agree that secondary sulfates are not harmful (including any secondary
aerosols which might not exist but for atmospheric processes involving
transformation of SO2) – a model run could nevertheless  be done based
on the assumption of little to no harm from these types of fine PM (with
as many caveats as EPA would like).  This would be of especial
significance for understanding the 14/35 option, which depends largely
on further reductions of SO2 from industry and EGUs.  What would the
costs and benefits of 14/35 be, if health effects of these types of fine
PM were negligible?

We would point out that DOE comments of May 1 on the Proposed Standard,
and DOE comments of July 6 on the Provisional Assessment, both reviewed
abundant new evidence showing that secondary sulfates and associated
organic aerosols are unlikely to cause much harm.  Most of these studies
have become available since the “cutoff date” of April 2002 for
consideration of new studies.  Thus there is adequate justification for
doing a provisional model run with the assumption that these types of
fine PM may pose negligible threats to human health.

For example, I became aware today of a new 2006 study, funded by EPA and
the Health Effects Institute, of the differential effects of types of
fine PM in Detroit.  This study finds that adverse airway responses in
allergic laboratory animals did not occur when the air mass was high in
fine PM mass and in secondary sulfate, but did occur on days with
smaller fine PM mass, but with higher levels of local emissions.  This
is another in a long line of studies making similar findings, most of
which have been provided to EPA and OMB in the two sets of prior
comments.

 Spatial Analysis of the Air Pollution-Mortality Relationship in the
Context of Ecological Confounders, J. Toxicol. Enviro. Health, Part A,
66: 1735-1777 (2003) 

 Geographies of Risk in Studies Linking Chronic Air Pollution Exposure
to Health Outcomes, , J. Toxicol. Enviro. Health, Part A, 68: 1-36
(2005)

 Chow et al, 2006 Critical Review Discussion: Health Effects of Fine
Particulate Air Pollution: Lines That Connect, J Air Waste Mgmt Assn, in
press (2006)

 Morishita, M. et al.  2006.  Source identification of ambient PM2.5
during summer inhalation exposure studies in Detroit, MI.  Atmospheric
Environment 40: 3823-3834

