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<p>Thank you!</p>
<p>regards, Ronald von Bayowahristan (where they are trying to
prohibit _all_ diesel vehicles, including passenger cars, from
driving through large cities.)</p>
<p><br>
</p>
<p><br>
</p>
<br>
<div class="moz-cite-prefix">On 10.09.2016 23:58, Traveller wrote:<br>
</div>
<blockquote
cite="mid:CAK27e=msjfsQcABGLayN=T--MdDi3f_ZuuvrL6=veVPNWnYOdg@mail.gmail.com"
type="cite">
<div dir="ltr">This too is a long post. "Take aways" for stovers
at the end. <br>
<br>
I have recently been diagnosed with many <a
moz-do-not-send="true"
href="https://www3.epa.gov/airquality/particlepollution/"
target="_blank">illnesses associated with PM2.5 </a>- aggravated
asthma, decreased lung function, and irritation of the airways,
coughing, and difficulty breathing.
<div><br>
Since I am a candidate for premature mortality, I decided to
poke around EPA web. <br>
<br>
-------------------------<br>
<br>
I began with <font
style="font-family:apertura-condensed-1,apertura-condensed-2,"helvetica
neue",helvetica,arial,"lucida
grande",sans-serif;line-height:1.6" size="2"><a
moz-do-not-send="true"
href="https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating"
style="font-family:apertura-condensed-1,apertura-condensed-2,"helvetica
neue",helvetica,arial,"lucida
grande",sans-serif;line-height:1.6" target="_blank">Carbon
Pollution Emission Guidelines for Existing Stationary
Sources: Electric Utility Generating Units</a> - A
proposed rule, 6/18/14, as part of the US Clean Power Plan
(which I otherwise generally like, science or no science).</font>
<div>
<div><br>
"These models assume that all fine particles, regardless
of their chemical composition, are equally potent in
causing premature mortality because the scientific
evidence is not yet sufficient to allow differentiation of
effect estimates by particle type."<br>
<br>
Whoa! This is justification by assumption!! <br>
<br>
I have serious doubts about whether air quality monitoring
stations in developing countries such as India adequately
capture all types of pollutants and are usable for
representative outdoor air pollution exposures, and
whether their design and use across the world is
appropriate for local conditions. <br>
<br>
But this makes me wonder where EPA's justification for
ambient concentration standards and achievement strategies
comes from. Ultimately its economics are in doubt - in
cost and benefit terms - though I grant once the standards
are set, economics may change. <br>
<br>
It gets worse:<br>
<br>
</div>
</div>
<blockquote style="margin:0px 0px 0px
40px;border:none;padding:0px">
<div>
<div>"<span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">In
this analysis, the EPA </span><span
style="font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"><font
color="#0000ff">assumes</font></span><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">
<u>that the health impact function for fine particles
is without a threshold</u>. This is based on the
conclusions of EPA's </span><i
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">Integrated
Science Assessment for Particulate Matter,</i><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"> </span><sup
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif"><a
moz-do-not-send="true" rel="footnote"
href="https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating#footnote-344"
style="border:0px;font-weight:inherit;font-style:inherit;font-size:13px;font-family:inherit;vertical-align:baseline;margin:0px;padding:0px;text-decoration:none;color:rgb(1,91,162)"
target="_blank">[344] </a></sup><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">which
evaluated the substantial body of published scientific
literature, reflecting thousands of epidemiology,
toxicology, and clinical studies that documents the
association between elevated PM </span><sub
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif">2.5</sub><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"> </span><span
style="border:0px;font-size:15.6px;font-family:athelas-1,athelas-2,georgia,serif;vertical-align:baseline;padding:0px;display:inline-block;width:11px;min-height:14px;color:rgb(54,54,54);line-height:25.2408px;background-image:url("http:///images/icons.png?1465417046");background-position:0px
-1045px;background-size:initial;background-repeat:no-repeat;background-origin:initial;background-clip:initial;background-color:initial"></span><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"><u>concentrations</u>
and </span><span
style="font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"><font
color="#0000ff">adverse health effects, including
increased premature mortality</font></span><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">.
This assessment, which was twice reviewed by the EPA's
independent Science Advisory Board, concluded that the
scientific literature consistently finds that</span><span
style="font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px"><font
color="#0000ff"> a no-threshold model most
adequately portrays the PM-mortality</font></span><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:15.6px;line-height:25.2408px">
<u>concentration-response relationship</u>." (Emphasis
added.)<br>
</span></div>
</div>
</blockquote>
<div>
<div><br>
What is "the relationship" between PM of any type and size
(2.5 and below) and how are these correlations arrived at
across different times, populations with different health
conditions and genetic makeup? <br>
<br>
What is being assumed constant in all the statistical
models that is hugely variable across populations and over
time? <br>
<br>
Inasmuch as PM2.5 concentrations may have declined in many
areas over the last few decades when these studies were
done and will continue to do so, why is EPA continuing
with some invariable relationship, even while admitting
that it is "less confident" (code for diffident, nervous)
in doing so? <br>
<br>
I quoted Burnett (2014) in an earlier post, "<span
style="font-size:12.8px">we are not suggesting that
there is convincing evidence that PM mortality and ALRI
risk is zero below any specific concentration based on
biological considerations (Brook et al. 2010). </span><u
style="font-size:12.8px">Absence of such evidence from
epidemiologic studies does not necessarily imply
evidence of the absence </u><span
style="font-size:12.8px">of such a counterfactual
concentration. We thus take the conservative approach
and set a positive counterfactual </span><wbr
style="font-size:12.8px"><span style="font-size:12.8px">concentration. However, our ap</span><wbr
style="font-size:12.8px"><span style="font-size:12.8px">proach can be adapted to a
different counterfactual if new evidence supporting a
positive association at lower
concentrations becomes availab</span><wbr
style="font-size:12.8px"><span style="font-size:12.8px">le."<br>
</span><br>
How can it be simultaneously the case that there is no
convincing evidence of a threshold (onetime, annual,
lifetime) for PM exposure for any particular population
AND that the "no-threshold model most adequately portrays
the PM-mortality concentration-response relationship."?<br>
<br>
Besides, note that EPA discusses only <u>"concentration-response"
relationship; we have moved far away from
"exposure-response relationships.</u><br>
<br>
Have data, will kill. </div>
<div><br>
</div>
<div>Assume emissions, assume concentrations (in the
developing world), and assume "concentration-response"
relationship. Voila! Another paper that EPA's next round
of Integrated Assessment for PM will review. The
Assessment will then be reviewed, maybe twice, by EPA's
independent (how can anything be EPA's and independent?)
advisory board? <br>
<br>
"Second-hand" science Ronald Fisher warned about is as
good as "second hand" second hand smoke. <br>
<br>
Literature review. Meta-analysis. These are tools of
deception. <br>
<br>
We have all joined Alice. <br>
<br>
----------<br>
<br>
</div>
</div>
<blockquote style="margin:0px 0px 0px
40px;border:none;padding:0px">
<div>
<div>
<p
style="border:0px;font-family:athelas-1,athelas-2,georgia,serif;vertical-align:baseline;margin:0px
0.4125em 0px 0px;padding:0px 0.2em
0.8125em;color:rgb(54,54,54);font-size:1.2em">"In
general, we are more confident in the magnitude of the
risks we estimate from simulated PM <sub>2.5</sub> concentrations
that coincide with the bulk of the observed PM
concentrations in the epidemiological studies that are
used to estimate the benefits. Likewise, we are less
confident in the risk we estimate from simulated PM <sub>2.5</sub> concentrations
that fall below the bulk of the observed data in these
studies.</p>
</div>
</div>
<div>
<p style="border:0px;vertical-align:baseline;margin:0px
0.4125em 0px 0px;padding:0px 0.2em 0.8125em"><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em">For
this analysis, <u>policy-specific air quality data
are not available,</u></span><u><sup
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em"><a
moz-do-not-send="true" rel="footnote"
href="https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating#footnote-345"
style="border:0px;font-weight:inherit;font-style:inherit;font-family:inherit;vertical-align:baseline;margin:0px;padding:0px;color:rgb(1,91,162)"
target="_blank"> </a></sup><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em">and
thus, we are unable to estimate the percentage of
premature mortality associated with this specific
rule's emission reductions at each PM</span><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em"> </span><sub
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em">2.5</sub><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em"> </span></u><span
style="color:rgb(54,54,54);font-family:athelas-1,athelas-2,georgia,serif;font-size:1.2em"><u>level</u>."<br>
<br>
</span></p>
</div>
</blockquote>
<div>
<p style="border:0px;vertical-align:baseline;margin:0px
0.4125em 0px 0px;padding:0px 0.2em 0.8125em">How reliable,
pray tell, are EPA's multi-decadal forecasts for PM2.5
(including dust, pollen, open burning, forest fires, some
of which are "natural") in the first place? Can everything
be controlled? <br>
<br>
<a moz-do-not-send="true"
href="https://www3.epa.gov/airquality/particlepollution/actions.html#dec12"
target="_blank">EPA says</a> that by 2020, even without
this Clean Power Plan, 99% of US counties (with monitors;
who cares when there is no monitoring) will meet EPA's
tightened 2012 standard of PM2.5. <br>
<br>
So, EPA knowingly computes health benefits and monetizes
them that it is "less confident" about. <br>
<br>
----------------<br>
<br>
It gets curiouser and curiouser. What <i>are</i> the new
<a moz-do-not-send="true"
href="https://www3.epa.gov/airquality/particlepollution/2012/decfsstandards.pdf"
target="_blank">(2012) EPA standards</a>? <br>
<br>
</p>
</div>
<blockquote style="margin:0px 0px 0px
40px;border:none;padding:0px">
<div>
<div>
<p style="border:0px;vertical-align:baseline;margin:0px
0.4125em 0px 0px;padding:0px 0.2em 0.8125em">"An area
will meet the standard if the <u>three-year average
of its annual
average</u> PM2.5 concentration (at each monitoring
site in the area) is less than or
equal to 12.0 µg/m3
." and " An
area meets the 24-hour standard if the <u>98th
percentile of 24-hour PM2.5
concentrations in one year, averaged over three
years</u>, is less than or equal to 35
μg/m3
." The PM10 standards, correspondingly are, "An area
meets the 24-hour PM10 standard if it does not exceed
the 150 µg/m3
level
more than once per year on average over a three-year
period."</p>
</div>
</div>
</blockquote>
<div>
<div>
<p style="border:0px;vertical-align:baseline;margin:0px
0.4125em 0px 0px;padding:0px 0.2em 0.8125em"><br>
So, all you have is an average of averages at monitoring
sites, particular locations heights that may or may not
correspond to human exposures. No matter;
concentrations, not exposures, kill. By EPA fiat. <br>
<br>
In developing countries, the spotty air quality monitors
do not even measure arguably more toxic pathogens from
open wastes, chemical spills, rural fires and dust
storms (except when they are transported to these holy
shrines of air pollution religion.) <br>
<br>
If EPA's concentration standard has fuzzy justification,
what's the point of source emission standards? Just air
basin modeling? <br>
<br>
How many 30-year forecasts for air quality and premature
mortality have been made in the last forty years, and
what is the record so far? <br>
<br>
Oops, the rates and composition of incidence of disease
have changed and arguably exposures have changed in a
way different from concentrations, so all of this is
forward-looking promises of a securities trader. <br>
<br>
Sub-prime regulation based on concocting false
assurances? <br>
<br>
-------------------------<br>
From what I see here as jiggery-pokery, I am relieved. I
could die any time but probably not from PM2.5
concentrations in Washington, DC. <br>
</p>
<div>I wonder if some scientists would call this
bankruptcy of science in the service of regulatory zeal,
climate change mania? <br>
<br>
Dick Schmalensee and Bob Stavins, in their 2013 paper <a
moz-do-not-send="true"
href="http://web.mit.edu/ceepr/www/publications/reprints/Reprint_248_WC.pdf"
target="_blank">The SO2 Allowance Trading System:The
Ironic History of a Grand Policy Experiment</a>*
concluded: "The central purpose of the SO2 allowance
trading program was to reduce the the
acidification of forest and aquatic ecosystems.. The
goal of reducing SO2 emissions was met and exceeded.
However, it turns out that the ecological benefits of
the program have been relatively small, largely because
it takes much longer than thought to reverse the
acidification
of ecosystems .. On the other
hand, other completely unanticipated benefits of the
program have been massive."<br>
<br>
My cynical re-reading of history - which I observed
first and second-hand - is that the central drivers of
that grand policy experiment were political - a)
ideological opposition to coal, no matter what the
merits; lb) Washington power struggle between coal
states of Appalachia and Illinois Basin versus coal
states of the West; and, c) power struggles between gas
and coal interests, groups within the coal interests,
and all the ancillary enterprises. </div>
<div><br>
</div>
<div>Schmalensee and Stavins (who might have been in the
White House CEQ at the time of the "acid rain" debates
and the "allowance trading" compromise compared to EPA's
earlier obsession with NSPS) further write <br>
<br>
</div>
</div>
</div>
<blockquote style="margin:0px 0px 0px
40px;border:none;padding:0px">
<div>
<div>
<div>"..but instead with human health impacts of
reduced levels of airborne fine sulfate particles less
than 2.5 micrometers in diameter
(PM ter (PM2.5), particles which derive from SO2
emissions. Epidemiological evidence
of the harmful human health effects of these fine
particulates mounted rapidly in
the decade he decade after the CAAA was enacted ....
human health benefits of the program may have exceeded
annual costs by a factor of more than fifty! With its
mandated
50 percent cut in SO2 emissions, the government did
what turned out to be the
right thing for the wrong reason."</div>
</div>
</div>
</blockquote>
<div>
<div><br>
</div>
<div>"Right thing"? These are all imputed benefits by
assumption loaded on assumption. There is no evidence that
actual health costs - disease treatment, lost days of
work, even death - declined compared to some baseline
estimate prior to 1995. Besides, the environment changed -
air and water quality - as did the populace - aging,
immigrants, internal migration, new housing stock.<br>
<br>
When your religion says that concentrations kill - damn
exposures - then you only need to assume that emissions
anywhere change concentrations everywhere, and voila, you
have saved people! <br>
<br>
Burnett (2014) have already told us the limits of
epidemiological evidence, and deployment of fancier models
with more restrictive assumptions in order to come up with
"relative risk"; further explorations are required. </div>
<div><br>
</div>
<div>--------------<br>
Now I am beginning to wonder whether the "epidemiological
evidence" was simply "evidence by assumption" and "changed
circumstances" that <u>required assuming that PM2.5
exposure was equally toxic no matter what species</u>. </div>
<div><br>
</div>
<div>Because, as the "acid rain" amendments to the Clean Air
Act (1990) required, SO2 emissions fell. A further boost
was provided by higher utilization factors of the US
nuclear power fleet. Presumably, local concentrations also
fell. <br>
<br>
With lower sulfates in the air, <b>did EPA scientists
need to assume equitoxicity in order to keep using old
data on concentration-response "relationship"</b>? <br>
<br>
Then, if equitoxicity was not enough in predicting
premature mortality and valuation of statistical lives
lost - EPA now recommends about $9 million as Value of
Statistical Life (<a moz-do-not-send="true"
href="https://www.epa.gov/environmental-economics/mortality-risk-valuation">$7.4
million in 2006$</a>; I inflate to the present) -<b> did
it need to also assume "no threshold" to raise
mortality?. </b><br>
<br>
Killing by assumption is lucrative. Evidence of absence is
a convenient untruth. <font face="georgia, times new
roman, times, serif" color="#000000"> </font></div>
<div><br>
-------------<br>
EPA has learnt a lesson from the acid rain program:
promises to "save lives" sell better than promises to
restore ecosystems. (I can make a model with synergies to
contradict this; ready to write a grant proposal to EPA?) <br>
<br>
"Premature mortality avoided" is the yardstick by which
EPA justifies its regulatory reach. <br>
<br>
By EPA's calculation, climate change action has <a
moz-do-not-send="true"
href="http://www.cnsnews.com/news/article/penny-starr/epa-chief-fighting-climate-change-could-prevent-69000-deaths-pollution-2100">annual
benefit of 69,000 deaths averted by 2100.</a> That
could be worth $7 trillion a year by 2100. (In 2100$, that
is. I assume VSL will rise to $100 million in 2100, with
inflation and higher productivities, i.e., higher GDP.) <br>
<br>
(I don't know how VSL factors in YLL. My premature death -
on the basis of average life expectancy for a Gujarati
male born in 1950s and properly vaccinated - will have
fewer YLL than that compared to GBD's new universal health
target - all deaths before age 86 are "premature". I am
willing to buy DALY reduction.) <br>
<br>
The Bush EPA failed to convince the US <a
moz-do-not-send="true"
href="https://www.supremecourt.gov/opinions/06pdf/05-1120.pdf">Supreme
Court</a> - save Antonin Scalia, who has suffered a
premature death, and John Roberts (still around) - that
CO2 molecules are not weapons of mass destruction. <br>
<br>
Then the Obama EPA made an "<a moz-do-not-send="true"
href="https://www.gpo.gov/fdsys/pkg/FR-2009-12-15/pdf/E9-29537.pdf">endangerment
finding</a>" with respect to climate change, that "the
air pollution is the combined mix of six
key directly-emitted, long-lived and
well-mixed greenhouse gases
(henceforth ‘‘well-mixed greenhouse
gases’’), which together, constitute the
root cause of human-induced climate
change and the resulting impacts on
public health and welfare."<br>
<br>
However, I could find only one specific reference to
premature mortality - to do with groundlevel ozone, which
is of course a potent warmer. There's much on
temperature-related mortality - unclear evidence on net
morbidity (heat v. cold) - and reference to
aero-allergens/temperature (no basis for judgment). The
primary culprit is ozone (whose precursors are sometimes
coemitted with PM, as is the case with inefficient solid
fuels use). <br>
<br>
It is interesting to see how the concept of "contribution"
is seen in legal terms. (I see "attribution" analogous to
"contribution" but I haven't done the legal research for
that.) EPA says, </div>
</div>
<br>
<blockquote style="margin:0px 0px 0px
40px;border:none;padding:0px">
<div>
<div>"In upholding EPA’s PM2.5 attainment
and nonattainment designation
decisions, the DC Circuit analyzed CAA
section 107(d), which requires EPA to
designate an area as nonattainment if it
‘‘contributes to ambient air quality in a
nearby area’’ not attaining the national
ambient air quality standards. Id. at 35.
The court noted that it had previously
held that the term ‘‘contributes’’ is
ambiguous in the context of CAA
language. See EDF v. EPA, 82 F.3d 451,
459 (DC Cir. 1996). ‘‘[A]mbiguities in
statutes within an agency’s jurisdiction
to administer are delegations of
authority to the agency to fill the
statutory gap in reasonable fashion.’’
571 F.3d at 35 (citing Nat’s Cable &
Telecomms. Ass’c v. Brand X Internet
Servs, 545 U.S. 967, 980 (2005)).
<u>The court then proceeded to consider
and reject petitioners’ argument that the
verb ‘‘contributes’’ in CAA section
107(d) necessarily connotes a significant
causal relationship</u>. S<u>pecifically, the DC
Circuit again noted that the term is
ambiguous, leaving it to EPA to
interpret in a reasonable manner. In the
context of this discussion, the court
noted that ‘‘a contribution may simply
exacerbate a problem rather than cause
it </u>* * * ’’ 571 F.3d at 39. This is
consistent with the DC Circuit’s
decision in Bluewater Network v. EPA,
370 F.3d 1 (DC Cir. 2004), in which the
court noted that the term contribute in
CAA section 213(a)(3) ‘‘[s]tanding alone,
* * * has no inherent connotation as to
the magnitude or importance of the
relevant ‘share’ in the effect; certainly it
does not incorporate any ‘significance’
requirement.’’ 370 F.3d at 13. The court
found that the bare ‘‘contribute’’
language invests the Administrator with
discretion to exercise judgment
regarding what constitutes a sufficient
contribution for the purpose of making
an endangerment finding. Id. at 14. " From <a
moz-do-not-send="true"
href="https://www.gpo.gov/fdsys/pkg/FR-2009-12-15/pdf/E9-29537.pdf">here</a>.<br>
<br>
</div>
</div>
</blockquote>
<div>
<div>Contribution does not necessarily connote a causal
relationship. </div>
<div><br>
</div>
<div>I suspect the same is true of attribution; not
necessarily a causal relationship. </div>
<div><br>
</div>
<div>GACC/IEA propaganda to the contrary. Relying on state
of the law so far. (Like emissions, law changes.) <br>
<br>
-----------------------------------<br>
<b>Lessons for us stovers: </b><br>
<br>
1. Do not get too anxious that "dirty cooking" kills. What
kills whom how is never that clear to doctors, and the GBD
statements about "attributable to risk factors" are
allegations in evolution. </div>
<div><br>
</div>
<div>2. There is no evidentiary basis to assume equitoxicity
and "no threshold" for PM2.5. At least, not for the air
pollution concentrations and composition found in poor
households for whom we debate "clean cooking." <br>
<br>
3. Just because EPA has shifted from "exposure-response"
to "concentration-response" does not mean everybody
everywhere has to fall for the emissions ->
concentrations -> death theology. At least, no promises
of "saving lives" are worth a statistical US life. </div>
<div><br>
</div>
<div>4. Insist on a long-term concentration profile, even if
exposures aren't measured, instead of the EPA/ISO
gobbledygook about emission RATES (whether lab or field
tests). Concentration data have to include all air
pollutants from all sources in specific environments, not
this WHO gaming with stove emissions. </div>
<div><br>
</div>
<div>5. Then there're additional problems of keeping all
risk factors unchanged (my prior post), confounding bias,
and the diversity among humans according to their genetic
basis, physical environments (agroclimatic zones, dwelling
type, transport). </div>
<div><br>
</div>
<div>6. Beware of US politics. EPA is becoming an Empire
Promotion Alliance. <br>
<br>
I am afraid what Cecil calls "fundamental foolishness" is
a diversion from more relevant research and planning issue
- air quality and exposure management strategies of the
conventional variety. We cannot pretend that the last 60
years of air management - science, economics, spatial
planning, buildings design - is worthless and "new source
voluntary performance targets" will save our sisters,
daughters, grand daughters. </div>
<div><span style="font-size:12.8px"><br>
Not that emission rates are entirely irrelevant. </span></div>
<div><span style="font-size:12.8px"><br>
</span></div>
<div><span style="font-size:12.8px">In air quality
strategies, reduction in emission rates - by source
type, stationary or mobile, small or large - is but one
of the means of lowering concentrations to standards and
presumably dosage and hence damage. For large stationary
sources with continuous emissions, usually a daily
average is specified for some pollutants (e.g. SO2). But
with small sources like household cookstoves - which can
vary enormously in fuel quality and operating practices
- a per minute max or a 15-minute max would seem to be
an appropriate metric, along with some hourly average
max. </span><br>
</div>
<div><br style="font-size:12.8px">
<span style="font-size:12.8px">I remember the
controversies on SO2 or low-level ionizing radiation, or
other pollutants from sources large and small, and how
the averaging times, maximum one-time and lifetime
exposures were incorporated in the standards for
equipment design or operations. But all that was real
epidemiology of cause and effect. With all this
cookstoves stuff, all you have is "premature deaths", a
statistical artifact for allocating across other
statistical artifacts called "risk factors". A premature
death is not a death, and a risk factor is not a
disease. Risk factors certainly contribute to diseases
and deaths, the causality links for which are sometimes
quite vague, at least debatable.<br>
<br>
Nikhil </span><span style="font-size:12.8px"> <br>
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<div><font
face="georgia,
serif">------------------------------<wbr>------------------------------<wbr>------------<br>
Nikhil Desai</font></div>
<div><font
face="georgia,
serif">(US <a
moz-do-not-send="true"
href="tel:%2B1%29%20202%20568%205831" value="+12025685831"
target="_blank">+1)
202 568 5831</a><br>
<i>Skype:
nikhildesai888</i><br>
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