[Stoves] Noise pollution and premature mortality

[Nikhil Desai]

Crispin:

You have brought this discussion back from noise pollution to PM2.5
pollution by solid fuel stoves, so it is no longer "off-topic".

I didn't find the EEA and WHO claims on "premature mortality from noise
pollution" extraordinary at all, just curious about their sources of energy
data to compute Leq.

I don't know about noisy versus quiet stoves -- except the Primus pressure
stove versus Nutan or Umrao wick kerosene stoves in my childhood - but all
you have to do is measure dB in some lab test, with an "adjusted" WBT
protocol. It doesn't matter what the background noise is, and how it
changes, nor even that your data is for different populations
(age/sex/geography/geneology) or outside the 55-80 dB range.

Just claim to have done some meta-analysis and then use the "hypothetical
exposure–response relationship between noise level (Ldn) and risk of
cognitive impairment" and linear extrapolation as used by the EEA and/or
WHO - i.e., IHME.

You ask "Is it true that the first assumption about solid fuels, that they
are ‘dirty’, is being validated by the numbers derived from that self-same
assumption?"

It's not even that. To call solid fuels "dirty", there have to be some
notion of what the emission rates are and what the consequences are, what
the pathways are. When you are looking at the 4+ billion life-years
(including lost, and of those who have died "post-maturely) of the human
cohort that died in 2015, there is no specific assumption I have yet been
able to trace in the public domain about fuel quality and quantity,
emission rates, concentrations, exposures, disease profiles, or deaths.

You see, appearances to the contrary, there is no "bottom up" model of
emissions to morbidity. Rather, GBD is a "top down" Blame Allocation Tool
(BAT).

Quite batty, you might say. There is "no there there". I know Jim Jetter
and Kirk Smith did a paper on developing emission estimates and referred to
some tests. But tests are not measurements of actual use by 3 billion
people. ready to be sacrificed at the "premature mortality" cult of IHME
and WHO.

No doubt, there are many scattered measurements of HAP - emission rates,
concentrations, - by experiments. I haven't totaled up the 2011 WHO
"emissions database" literature about how many people in total, when and
where, but this is an old industry of experiments.

Experimental data are not applicable to the world at large with the huge
diversity across geographies and cultures, over time, among the 4 million
premature deaths attributed to HAP. That is HAP hype. I plead totally
agnostic; all I see in the "top down" exercise is some references to
satellite data (not very good for the depth of opacity) and global
circulation models, plus indefensible assumptions of equitoxicity and the
Inttegrated Exposure Response. As far as I know, the cooked up premature
mortality data have NOT been used to validate these assumptions. That would
be too transparent a deceit.

I don't care how many premature deaths are attributed to noise or PM2.5 or
indecent exposure or violating God's Law or papal commands. All I care is
the predictability and policy relevance. I re-assert that these are ZERO.

More later if you wish on the commonality between noise pollution and air
pollution DALY cakes.

Nikhil

On Wed, Jul 26, 2017 at 3:38 PM, Crispin Pemberton-Pigott <
crispinpigott at outlook.com> wrote:

> Dear Nikhil
>
> This is absolutely extraordinary. You mean I can get aDALY credits for
> changing a noisy (they are called Roarer heads for a reason) kerosene stove
> to a quiet and serene wood pellet stove?
>
> I would never have guessed that. I can even save the children. Who knew?
>
> I am interested in the assumptions that lie behind the models for a simple
> reason: if an assumption, called ‘A’, is made, and then various modeling of
> exposure and effects is delivered into a model of health consequences, at
> some point the result could be used to ‘create’ the claim that based on the
> modeled health effects ‘B’, ‘A’ is a fact. Maybe I should write ‘fact’
> because that would a carefully constructed and cleverly hidden loop where
> ‘A’ leads to health consequence ‘B’ which as a stand-alone number, can be
> used to claim that ‘A’ must be true because ‘B’ is true and leads to ‘A’.
>
> Isn’t that what is happening? Is it true that the first assumption about
> solid fuels, that they are ‘dirty’, is being validated by the numbers
> derived from that self-same assumption?
>
> Thanks for your attention to details
> Crispin
>
>
>
>
> Crispin:
>
> Your news on UK solid fuel stoves led me to another article on the same
> webzine - EU warning over air quality outlook<http://www.airqualityn
> ews.com/2015/03/03/eu-warning-over-air-quality-outlook/> 3 March 2015.
>
> The European Environment Agency is quoted as saying,
>
> "Road traffic is considered the greatest contributor to noise exposure in
> Europe, and most recently the EEA estimates that environmental noise
> contributes to around 10,000 premature deaths due to coronary heart disease
> and stroke each year."
>
> That's Europe-wide and for 2011. I am glad to see WHO Europe imprimatur. I
> quote from WHO Europe Burden of Disease from Environmental Noise<
> http://www.euro.who.int/__data/assets/pdf_file/0008/136466/e94888.pdf>
> (2011)
>
> "Exposure–response relationship
>
> For a quantitative risk assessment and the derivation of guidelines for
> public health noise policy, a common exposure–response curve is required.
> The risk estimates obtained from different noise studies can be summarized
> using the statistical approach of meta-analysis.
>
> Definition of exposure
>
> Energy-based indicators of exposure (Leq) are adequate and sufficient for
> assessing the relationship between long-term exposure to community noise
> and chronic diseases such as cardiovascular disorders. While single event
> noise indicators can be useful predictors (as additional information) for
> assessing the effects of acute noise (e. g. sleep disturbance) (112),
> integrated noise indicators (e.g. a year’s average noise level) are
> suitable predictors in epidemiological studies for assessing the long-term
> effects of chronic noise exposure."
>
>
> Leq is "weighted equivalent sound pressure level" over certain hours (4
> hours for night-equivalent and 12 hours for day-equivalent".
>
> I don't see how Leq are computed from "energy" data except that diesel
> sales to construction and landscaping industry may be used to compute some
> noise levels using "noise emission factors". And maybe small industry
> surveys and power plants can also do the same. Lawn mowers and tree cutters
> are the most significant noise I hear these days, apart from the keyboard
> clicks (sure to cause premature death).
>
> No matter, they have a dose-response curve from meta-analysis. As reported
> in the Executive Summary:
> Cardiovascular diseases
>
> The evidence from epidemiological studies on the association between
> exposure to road traffic and aircraft noise and hypertension and ischaemic
> heart disease has increased during recent years. Road traffic noise has
> been shown to increase the risk of ischaemic heart disease, including
> myocardial infarction. Both road traffic noise and aircraft noise increase
> the risk of high blood pressure. Very few studies exist regarding the
> cardiovascular effects of exposure to rail traffic noise.
>
> Exposure–response relationships
>
> Numerical meta-analyses were carried out assessing exposure–response
> relationships between community noise and cardiovascular risk. A polynomial
> function was fitted through the data points from the analytic studies
> within the noise range from 55 to 80 dB(A):
>
>  Estimated burden in western Europe
>
> Based on the exposure data from the noise maps of EU Member States, it is
> estimated that the burden of disease from environmental noise is
> approximately 61 000 years for ischaemic heart disease in high-income
> European countries.
>
> Cognitive impairment in children
>
> The case definition of noise-related cognitive impairment is: The
> Reduction in cognitive ability in school-age children that occurs while the
> noise exposure persists and will persist for some time after the cessation
> of the noise exposure. The extent to which noise impairs cognition,
> particularly in children, has been studied with both experimental and
> epidemiological studies.
>
> Hypothetical exposure–response relationship
>
> Based on available evidence, a hypothetical exposure–response relationship
> between noise level (Ldn) and risk of cognitive impairment was formulated:
> all of the noise exposed children were cognitively affected at a level as
> high as 95 dB(A) Ldn, and no children were affected at a relatively low
> level, such as 50 dB(A) Ldn. A linear relationship in the range of these
> two limits was assumed as a basis for a conservative approximation of YLD.
>
> Estimated burden in western Europe
>
> If one extrapolates the exposure distribution and population structure of
> Sweden to western European countries, the estimated DALYs for the EUR-A
> countries are 45 000 years for children aged 7–19 years.
>
> There are striking parallels to the "data free", "reality free" war on
> solid fuels by WHO's "Global Burden of Disease from Air Pollution".
>
> The GBD cult must declare that GBD has zero predictive value. Which means
> zero policy relevance.
>
> Failing which, you and I can develop $/aDALY scheme for our advanced
> noise-blocking glass technology for buildings.
>
> Nikhil
>
>
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