Here is a silly NYTimes reporter’s analysis of the risk of breathing small particle-tainted air. As Milloy always says–show us the bodies. No fair just counting deaths, got to do a medical investigation.
Ok so start with small particles that come from cigarettes, agricultural activity, industrial activity, internal combustion engines–lots of different sources, probably of different toxicity, No?
The EPA and its running dog researchers do observational studies that are worthless, since they show small associations in the context of uncontrolled and even unknown confounders and monitors that only measure particles by size.
Then they just do the Cargo Cult game of authoritative number crunching for “associations” and blow smoke about small associations.
They harvest daily death count variations and claim a signal for toxic causation. Sure it is.
They claim a small particle premature death effect at a lag time of 1 or 2 or 3 days. That’s why I have never seen such a death–it’s a number derived from counting deaths, not investigating them. Killing people in a couple of days? Really? Even if the small particles exposure was very toxic, I could keep somebody severely and lethally damaged alive for a long time on a ventilator–what’s the answer to that?
Milloy always points out the basic problem of unknown exposures for death counts. Outside, inside, as a clear problem with the studies that run on outside air monitors when people are indoors more than 80 percent of the time. Another confounder that can’t be eliminated.
Toxicologists always point out that small particle is size, and doesn’t determine toxicity assuming that all sources are toxic ignores basic toxicology. Weaponized anthrax dust is similar in particle size to talcum powder. Agricultural dust can’t possibly be the same toxicity as industrial source emissions? Get the point?
Note that the claims of deaths based on the junk science projections range into the millions for small particles with no attempt to really determine what’s premature, or what was the nature of the exposure or the toxicity of the small particle load inhaled.
Of course you might also note the loose use of “premature” deaths. The researchers don’t do life expectancy analysis for the deaths.
And so now we have something that completely overwhelms the pea sized brain of a journalist who doesn’t understand toxicology and epidemiology and how the EPA researchers lie. However he does know the claims of deaths and he knows air pollution bad, smoking bad.
All the premature deaths studies that are the basis of EPA claims made to the US Congress that they are trying to stop hundreds of thousands of deaths each year from small particles are flawed and misuse the concept of premature death. The studies are counting deaths and matching elevated death rates against air pollution monitor reports, without regard to exposure confounding or even life expectancy. The researchers are harvesting the variability of death rates against computer dredging for a corresponding blip in small particle reports.
Smoking Risk
Cigarette smoking results in a pack/year increase in lung cancer so lifetime smokers have a 10 % risk of lung cancer, and the Relative Risk (RR) for smokers is 900 % or an RR of 10. It is time sensitive though, so if you stop smoking your RR will return to close to non smokers, if you stop soon enough, like before 10 years. The amount smoked is important–dose does make the poison.
Second hand smoking even in the data tortured meta analyses of the EPA and the Surgeon General shows an RR of 1.2 and yet they claim one breath of SHS is deadly–sure thing when you’re on a roll you can claim anything, its called lying for justice in politics or lying for a cause in the nanny state. Can’t be too careful–a good scare will have the right effect on behavior even if exaggerated. Precautionary principle kicks in. Some studies show no risk at all for second hand smoke (shs), environmental tobacco smoke(ets) so then the question is does one study refute a stack of studies that use bad methodology?
Here is a fine discussion by the Milloy
http://junkscience.com/2012/12/03/whats-epa-smoking/
Human exposure experiments
The EPA authorized and funded human exposure experiments with small particles at 10 domestic medical research facilities, 9 of them medical schools. Imagine Human exposure experiments with substances claimed by the sponsor to be lethal and carcinogenic.
Milloy and I were involved in investigating the human experiments and the filing of a lawsuit to stop them, American Traditions Institute v EPA.
Our position was why would the EPA sponsor and fund human exposure experiments with small particles when the EPA administrator said in testimony before congress that small particles were lethal and caused hundreds of thousands of deaths in America every year. Jon Samet MD said that there is no safe level of small particles, and he is the Chair of the Clean Air Scientific Advisory Committee of the EPA.
Robert Devlin, PhD, lead researcher at the North Carolina Lab that was doing human exposure experiments specified in the lawsuit, explained why the EPA was doing human exposure experiments.
From para 1 of his Declaration under penalty of perjury
“I am a Senior Scientist (ST) for the Environmental Public Health Division (EPHD), National Health and Environmental Research Laboratory (NHEERL), Office of Research and Development (ORD), U.S. Environmental Protection Agency. As one of three STs in NHEERL I am expected to be a scientific leader in the area of air pollution research, to define important areas of research, assemble teams to carry out that research and ensure it is completed in a timely manner and published in peer-reviewed journals. I am currently on detail as Acting Associated Director for Health for NHEERL. Prior to my current position, I was Chief of the Clinical Research Branch (CRB) of the EPHD from 1994 – 2008. The CRB is responsible for doing nearly all controlled human exposure studies within NHEERL.”
Then from para 7 and 8 of the same declaration.
“Epidemiological observations are the primary tool in the discovery of risks to public health such as that presented by ambient PM2.5. However, epidemiological studies do not generally provide direct evidence of causation. They indicate the existence or lack of a statistical relationship between ambient levels of PM2.5 and adverse health outcomes. Large population studies cannot assess the biological mechanisms (called biological plausibility) that could explain how inhaling ambient air pollution particles can cause illness or death in susceptible individuals. This sometimes leaves open the question of whether the observed association in the epidemiological study is causal or whether PM2.5 is merely a marker for some other unknown substance.
8. Controlled human exposure studies conducted by EPA scientists and EPA funded scientists at multiple universities in the United States fill an information gap that cannot be filled by large population studies.”
Back to Second Hand Smoke.
The studies on non smoking spouses of smokers have never shown an adequate relative risk association for evidence of carcinogenicity. The EPA and the smoking ban forces use faulty studies to push a strategy to stop smokers and stigmatize smokers as a toxic nuisance.
The smoking ban forces just pound the table in the absence of good evidence of toxicity and carcinogenicity of Second Hand Smoke.
It is not surprising that the NYT can’t get it right. An army of junk scientists has been working for more than 2 decades to create a smoky (pardon the pun) environment for evaluating air pollution and second hand smoke toxicology.
here’s the way we look at it.
that is the milloy and me–and people who agree with us.
dust and small particle air pollution of other kinds from other sources, do have the ability to get past the medium sized brioncholes down into the lung farther.
so the first rank of airways is bronchi, in adules more than a cmin diameter, then you get into various smaller and amsller bronchioles down to the terminal bronchiole that opens into the air sacs with blood vessels for gas exchange called the alveoli–alveoli is the functional part of the lung very small sacs with blood vessels in the walls.
Important to note that in the middle sized airways there are filimentous cilia that beat and move the mucous and junk from the lung to a place where it can go out. lung damage reduces those cilia.
Emphysemais destruction of the innard membranous soft tissue of the lung so big bubbles develop. chronic bronchitis is inflammation of the airways, and bronchiectasis is development of areas of intense infection that destroyes lung tissue and sets up a chronic infection. lung abscess is usually from inhaling something and causes just a regular abscess, fibrotic or caseating disease of the lungs is from self destruction or from agents that cause inflammatory processes.
so lung cancer is airway cancer or alveolar cancer, or pleural (capsule around the lung) cancer, usually mesothelioma.
the cancer that is most common is squamous cell, derivative of the flat protective cells of the bigger airways–probably irritation and chronic damage cause squamous cell, adeno is cancer of the cells that are columnar and I am not going to presume too much except the adeno cancer comes from airway cells deeper in the airways. adeno arises from the airways too, and probably could be blamed on irritation and chronic damage.
alveolar cell cancer is more rare and then also rare is pleural cell cancer, notoriously associated with exposure to the nasty form of asbestos, the blue and dark form, white being less likely because it doesn’t get so far down.
so the reason that smokers have a 900 % increase in lung cancer risk is that after years of irritation from smoking, the cells go wild–it isn’t easy to say why things go wild and abnormally replicating lines of cells develop.
one thing that is a misunderstanding is that cancer cell lines are not so much mutational, as polyploidic–they have greater than the normal set of chromosomes. we don’t really understand cancer that well.
there is no evidence to support the assertion that small particles cause cancer, like smoking does or asbestos does.
none.
There is no ambient small particle pollution that comes close to the intensity of small particles in inhaled cigarette smoke. There is no scientific evidence that ambient small particle air pollution causes premature death–they find RR of less than 1.1. That’s our point.
24 mics/cubic meter is the EPA short term safety level for small particles.
inhaled cig smoke is much more than 1000 mics. much more.
the chinese air when its really bad is 500-600 mics/cubic meter as I recall.
dose makes the poison. ,
John Dale Dunn MD JD Consultant Emergency Services/Peer Review Civilian Faculty, Emergency Medicine Residency Carl R. Darnall Army Med Center Fort Hood, Texas Medical Officer, Sheriff Bobby Grubbs Brown County, Texas 325 784 6697 (h) 642 5073 (c)
Ah, good. Thank you for letting us know. My detector of the unusual has been firing for a while. I reckon, Steve did not take a break from JunkScience for about 20 years.
I like the part about no known minimum exposure that is not lethal and death from exposure in a couple of days. Doesn’t that rather fly in the face of casual observation?
I bet if you could collect opinions just before death, a very high percentage would be of the opinion that their death was premature.
Steve is fine, in fact he contributed to the NYT piece in a number of valuable ways.
John Dale Dunn MD JD Consultant Emergency Services/Peer Review Civilian Faculty, Emergency Medicine Residency Carl R. Darnall Army Med Center Fort Hood, Texas Medical Officer, Sheriff Bobby Grubbs Brown County, Texas 325 784 6697 (h) 642 5073 (c)
By the way, where is Steve? Is he all right?
There are easily identifiable believables at play here. From obituaries, we know that all deaths are premature. From everyday experience, we know that dust wreaks havoc with mechanisms. Got a torn dust boot on your CV joint? Get ready to replace the joint soon. Projecting this kind of experience onto biological mechanisms does not require a strenuous effort.
The only difference is, life tends to repair itself. How efficient are our repair mechanisms vis-a-vis fine particulates we encounter every day? I don’t know. I have been asking myself since I was 6, when wise grown-ups alerted me to the idea that beating up clouds of dust while playing in a sandbox could shorten my life. That was a strange idea, but it sounded mysterious enough and I remembered it. When I was 12, a pathologist told me there was no natural repair available for black lung. He showed me the lungs of dead smokers and dead miners (all miners back then were smokers, so it was a bit hard to know what did them in). I know pathologists tend to err on the gloomy side. You have a gross sample and a dead body; connect the dots. Their musings and samples I was shown did impress me: I developed a habit of covering my breathing holes with a tissue or holding my breath when exposed to visible dust. But there is a lot of invisible or hard-to-see stuff floating around (just shine a laser pointer). How much have I got and when is it going to kill me? No answer. Attempts by EPA don’t count. Not as bona fide attempts.
I do suspect though, that the old assertion about the absence of natural protection may not be correct. I personally know many people who have been far less careful than I am but far more exposed, and they are still in good health, now in their late 60s.