[Stoves] USEPA: Absence of evidence is evidence of absence (re: Ron on WHO webinar)
Ronald Hongsermeier
rwhongser at web.de
Sun Sep 11 11:27:04 CDT 2016
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 thata
> 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 <tel:%2B1%29%20202%20568%205831>
> /Skype: nikhildesai888/
>
>
>
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