[Stoves] USEPA: Absence of evidence is evidence of absence (re: Ron on WHO webinar)

[Traveller]

Ronald:

I didn't know where Bayowahristan is, so looked up on the web and
discovered Balawaristan is a historical name for Gilgit-Baltistan in
today's Pakistan. Good to know.

I happen to like the idea of prohibiting some diesel vehicles in some areas
- e.g. trucks in residential areas - for reasons additional to air
pollution, namely noise, safety hazards, clogging traffic. Small diesel
trucks for cargo could be ideal candidates for hybrid or battery.

Banning all diesel vehicles, including passenger cars, from driving through
large cities - what you mention - may also conceivably be a good idea, but
only as part of a regional air quality compliance strategy.

Obsessing over one type of source, its emission rates (and presumed annual
loads), without regard to other sources and types of pollutants or
historical and future exposure profiles, is regulatory overzeal.

When it comes to household stoves -- a piece in a complex system of cooking
and with deep behavioral patterns that may only be changed by a transition
to another fuel/stove combination - this obsession becomes laughable.

Still, clean enough stoves that users prefer - for reasons of convenience,
appearance, whatever - are worth working on, without regard to the ISO
"fundamental foolishness".

Who knows, even fools may pass tests. I have.

Nikhil


---------
(India +91) 909 995 2080

On Sun, Sep 11, 2016 at 12:27 PM, Ronald Hongsermeier <rwhongser at web.de>
wrote:

> Thank you!
>
> regards, Ronald von Bayowahristan (where they are trying to prohibit _all_
> diesel vehicles, including passenger cars, from driving through large
> cities.)
>
>
>
>
> On 10.09.2016 23:58, Traveller wrote:
>
> This too is a long post. "Take aways" for stovers at the end.
>
> I have recently been diagnosed with many illnesses associated with PM2.5
> <https://www3.epa.gov/airquality/particlepollution/>- aggravated asthma,
> decreased lung function, and irritation of the airways, coughing, and
> difficulty breathing.
>
> Since I am a candidate for premature mortality, I decided to poke around
> EPA web.
>
> -------------------------
>
> I began with Carbon Pollution Emission Guidelines for Existing Stationary
> Sources: Electric Utility Generating Units
> <https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating> -
> A proposed rule, 6/18/14, as part of the US Clean Power Plan (which I
> otherwise generally like, science or no science).
>
> "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."
>
> Whoa! This is justification by assumption!!
>
> 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.
>
> 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.
>
> It gets worse:
>
> "In this analysis, the EPA assumes *that the health impact function for
> fine particles is without a threshold*. This is based on the conclusions
> of EPA's *Integrated Science Assessment for Particulate Matter,* [344]
> <https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating#footnote-344>which
> evaluated the substantial body of published scientific literature,
> reflecting thousands of epidemiology, toxicology, and clinical studies that
> documents the association between elevated PM 2.5 *concentrations* and adverse
> health effects, including increased premature mortality. This assessment,
> which was twice reviewed by the EPA's independent Science Advisory Board,
> concluded that the scientific literature consistently finds that a
> no-threshold model most adequately portrays the PM-mortality *concentration-response
> relationship*." (Emphasis added.)
>
>
> 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?
>
> What is being assumed constant in all the statistical models that is
> hugely variable across populations and over time?
>
> 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?
>
> I quoted Burnett (2014) in an earlier post, "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). *Absence of such evidence from epidemiologic studies does not
> necessarily imply evidence of the absence *of such a counterfactual
> concentration. We thus take the conservative approach and
> set a positive counterfactual concentration. However, our approach can be adapted to a
> different counterfactual if new evidence supporting a positive association
> at lower concentrations becomes available."
>
> 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."?
>
> Besides, note that EPA discusses only *"concentration-response"
> relationship; we have moved far away from "exposure-response relationships.*
>
> Have data, will kill.
>
> 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?
>
> "Second-hand" science Ronald Fisher warned about is as good as "second
> hand" second hand smoke.
>
> Literature review. Meta-analysis. These are tools of deception.
>
> We have all joined Alice.
>
> ----------
>
> "In general, we are more confident in the magnitude of the risks we
> estimate from simulated PM 2.5 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 2.5 concentrations that fall below the bulk
> of the observed data in these studies.
>
> For this analysis, *policy-specific air quality data are not available,**
> <https://www.federalregister.gov/articles/2014/06/18/2014-13726/carbon-pollution-emission-guidelines-for-existing-stationary-sources-electric-utility-generating#footnote-345>and
> thus, we are unable to estimate the percentage of premature mortality
> associated with this specific rule's emission reductions at each PM 2.5 *
> *level*."
>
> 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?
>
> EPA says
> <https://www3.epa.gov/airquality/particlepollution/actions.html#dec12>
> 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.
>
> So, EPA knowingly computes health benefits and monetizes them that it is
> "less confident" about.
>
> ----------------
>
> It gets curiouser and curiouser. What *are* the new (2012) EPA standards
> <https://www3.epa.gov/airquality/particlepollution/2012/decfsstandards.pdf>?
>
>
> "An area will meet the standard if the *three-year average of its annual
> average* 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 *98th percentile of 24-hour PM2.5 concentrations in one
> year, averaged over three years*, 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."
>
>
> 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.
>
> 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.)
>
> If EPA's concentration standard has fuzzy justification, what's the point
> of source emission standards? Just air basin modeling?
>
> 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?
>
> 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.
>
> Sub-prime regulation based on concocting false assurances?
>
> -------------------------
> 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.
> I wonder if some scientists would call this bankruptcy of science in the
> service of regulatory zeal, climate change mania?
>
> Dick Schmalensee and Bob Stavins, in their 2013 paper The SO2 Allowance
> Trading System:The Ironic History of a Grand Policy Experiment
> <http://web.mit.edu/ceepr/www/publications/reprints/Reprint_248_WC.pdf>*
> 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."
>
> 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.
>
> 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
>
> "..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."
>
>
> "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.
>
> 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!
>
> 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.
>
> --------------
> Now I am beginning to wonder whether the "epidemiological evidence" was
> simply "evidence by assumption" and "changed circumstances" that *required
> assuming that PM2.5 exposure was equally toxic no matter what species*.
>
> 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.
>
> With lower sulfates in the air, *did EPA scientists need to assume
> equitoxicity in order to keep using old data on concentration-response
> "relationship"*?
>
> 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 ($7.4 million in 2006$
> <https://www.epa.gov/environmental-economics/mortality-risk-valuation>; I
> inflate to the present) -* did it need to also assume "no threshold" to
> raise mortality?. *
>
> Killing by assumption is lucrative. Evidence of absence is a convenient
> untruth.
>
> -------------
> 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?)
>
> "Premature mortality avoided" is the yardstick by which EPA justifies its
> regulatory reach.
>
> By EPA's calculation, climate change action has annual benefit of 69,000
> deaths averted by 2100.
> <http://www.cnsnews.com/news/article/penny-starr/epa-chief-fighting-climate-change-could-prevent-69000-deaths-pollution-2100>
> 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.)
>
> (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.)
>
> The Bush EPA failed to convince the US Supreme Court
> <https://www.supremecourt.gov/opinions/06pdf/05-1120.pdf> - save Antonin
> Scalia, who has suffered a premature death, and John Roberts (still around)
> - that CO2 molecules are not weapons of mass destruction.
>
> Then the Obama EPA made an "endangerment finding
> <https://www.gpo.gov/fdsys/pkg/FR-2009-12-15/pdf/E9-29537.pdf>" 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."
>
> 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).
>
> 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,
>
> "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)). *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*. S*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 ** * * ’’ 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 here <https://www.gpo.gov/fdsys/pkg/FR-2009-12-15/pdf/E9-29537.pdf>
> .
>
> Contribution does not necessarily connote a causal relationship.
>
> I suspect the same is true of attribution; not necessarily a causal
> relationship.
>
> GACC/IEA propaganda to the contrary. Relying on state of the law so far.
> (Like emissions, law changes.)
>
> -----------------------------------
> *Lessons for us stovers: *
>
> 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.
>
> 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."
>
> 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.
>
> 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.
>
> 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).
>
> 6. Beware of US politics. EPA is becoming an Empire Promotion Alliance.
>
> 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.
>
> Not that emission rates are entirely irrelevant.
>
> 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.
>
> 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.
>
> Nikhil
>
>
>
>
> ------------------------------------------------------------------------
> Nikhil Desai
> (US +1) 202 568 5831 <%2B1%29%20202%20568%205831>
> *Skype: nikhildesai888*
>
>
>
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