Acrolein in smoke suppresses the immune system

Research studies on wood smoke and other air pollution.

Acrolein in smoke suppresses the immune system

Postby Wilberforce » Sun Sep 13, 2009 10:00 pm

RESEARCH

Acrolein in cigarette smoke inhibits T-cell responses
Lambert, et al
http://www.jacionline.org/article/S0091 ... 2/abstract

"The potency and volatility of acrolein could also account for the apparent immunosuppressive effects of
passive smoke. A recent study of 4486 infants demonstrated a strong correlation between the incidence
of severe respiratory tract infections and the proximity of the child to cigarette smoke while nursing.
In addition, children infected with Mycobacterium tuberculosis are 5 times more likely to develop active
pulmonary tuberculosis if exposed to tobacco smoke. At a respiration rate of 2 to 4 L/min, a child could
theoretically receive an immunosuppressive dose of acrolein (~10-30 mg) from a 1-hour exposure to the
levels of second-hand smoke typically found in restaurants. Further research is therefore necessary to
identify biomarkers of acrolein exposure and to assess the pharmacodynamics of acrolein exposure."


Acrolein is present in significant quantities in wood smoke.

Up to 100 mg of acrolein is released by the combustion of one kilogram of wood.

_________________________________________________________________________________

REFERENCE

A Summary of the Emissions Characterization and Noncancer
Respiratory Effects of Wood Smoke-EPA-453/R-93-036

http://www.epa.gov/ttn/atw/burn/woodsmoke1993.pdf
_______________________________________________________________________________________

A T-cell is part of the body's immune system:
http://en.wikipedia.org/wiki/T_cell

_______________________________________________________________________________________

Related studies

Prioritization of Toxic Air Contaminants - Children’s Environmental Health Protection Act
http://oehha.ca.gov/air/toxic_contamina ... _final.pdf
Acrolein has been measured in smoky indoor air. In bars and restaurants, levels between
2.3 and 275 mg/m3 have been reported (IARC, 1995: citing Triebig and Zober, 1984; Löfroth
et al., 1989). In residences where wood stoves were used, concentrations from 0.7-6.0 mg/m3
have been reported (IARC, 1995: citing Highsmith et al., 1988).


Cigarette smoking as a risk factor for epidemic a(h1n1) influenza in young men
Kark, et al
http://content.nejm.org/cgi/content/abs ... 07/17/1042
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Re: Acrolein in smoke inhibits

Postby pm2.5mary » Fri Oct 02, 2009 10:39 pm

Good Sleuthing! Thank you for posting this important research! These papers fill an important gap. Now we still need to find a paper about the smoke particles also being vectors for bacteria and virus. We know this from testimony of live bacteria and virus found at altitudes of 1,000 feet. The soot particles' ability to absorb moisture and toxins makes a cozy home for disease causing organisms. Someone knows all about this, we need to find their work. I have not finished reading all of this yet. Very exciting...

Thanks again, yes, we will move this over to the website.
"Particulate pollution is the most important contaminant in our air. ...we know that when particle levels go up, people die. " (Joel Schwartz, Ph.D., Harvard School of Public Health, E Magazine, Sept./Oct. 2002)
Find more at http://burningissues.org
User avatar
pm2.5mary
 
Posts: 320
Joined: Sun Oct 15, 2006 6:04 pm

Re: Acrolein in smoke suppresses the immune system

Postby Wilberforce » Mon Nov 16, 2009 8:02 pm

EPA Monitoring Update: Acrolein
http://www.epa.gov/schoolair/pdfs/acroleinfs.pdf

Acrolein levels may be higher in areas near fires. If you’ve ever felt your eyes burn
when you were near a smoky fire, high levels of acrolein were most likely the cause.
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Re: Acrolein in smoke suppresses the immune system

Postby Wilberforce » Tue Dec 29, 2009 11:07 pm

Acrolein is a major cigarette-related lung cancer agent:
Preferential binding at p53 mutational hotspots and inhibition of DNA repair

Feng, et al
http://www.pnas.org/content/103/42/15404.abstract

From the full article (OPEN ACCESS)
"Acr is one of the most abundant compounds generated in CS; the amount of Acr in a single cigarette,
depending on the manufacturer, ranges from 10 to 500 μg. The total amount of PAHs present in CS,
in contrast, is in the range of just a few micrograms. Acr has been shown to interact with nucleophiles,
including DNA and proteins in cells. Unlike PAHs, where only metabolically activated forms can form
adducts with DNA, Acr can directly interact with DNA and form DNA adducts. Similar to PAH–DNA
adducts, Acr–DNA adducts induce mainly G:C-to-T:A transversion mutations, the major type of mutations
found in the p53 gene in CS-related lung cancer. Although the carcinogenicity of Acr in the lung has not
been studied because of the severe toxicity associated with Acr treatment in animals, i.p. injection of Acr
has been shown to cause bladder cancer in rats. These results indicate that Acr is indeed a carcinogenic
substance...These results strongly suggest that Acr–dG adducts, as well as PAH–DNA adducts, contribute
greatly to these mutations in lung cancer."
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Re: Acrolein in smoke suppresses the immune system

Postby pm2.5mary » Wed Dec 30, 2009 12:26 am

Thanks Woodnyet! Stocking up on science is the way to arm ourselves to stop wood smoke and wood burning for good in 2010.

Happy New Year! No wood burning allowed!
"Particulate pollution is the most important contaminant in our air. ...we know that when particle levels go up, people die. " (Joel Schwartz, Ph.D., Harvard School of Public Health, E Magazine, Sept./Oct. 2002)
Find more at http://burningissues.org
User avatar
pm2.5mary
 
Posts: 320
Joined: Sun Oct 15, 2006 6:04 pm

Re: Acrolein in smoke suppresses the immune system

Postby Wilberforce » Wed Dec 30, 2009 10:38 am

Thanks Mary. The reason I am blasting away at acrolein, is that I feel it may
be the chemical constituent in wood (and tobacco) smoke which has potentially
the most imminent effect on the lungs. And most importantly during this
flu season.
We hear of many H1N1 deaths across the country; one would
think people (if they were aware of the smoke/smoking/immune depletion effects)
would try to avoid any and all particulate matter and smoke. I always remind my
students to quit smoking and not to attend bonfires.

The same goes for cooking oils. For those working in restaurants and home
kitchens, acrolein vapor from overheated fats (as well as PM 2.5 and PM 10)
can build up in enclosed places. For example, my two brother-inlaw chefs
made a nice pork roast (by searing and braising). The searing part put a lot
of particulate in the air, of mostly the larger sizes. It may be cold up here,
but the windows had to be opened (I need an actual vent over my stove
to replace the faux one)

Here are some more acrolein-related studies, already posted in Science:

Exposure to Mutagenic Aldehydes and Particulate Matter During Panfrying
of Beefsteak with Margarine, Rapeseed Oil, Olive Oil or Soybean Oil

viewtopic.php?f=15&t=1582

Increased Susceptibility and Severity of Influenza in Mice Exposed to Diesel Exhaust.
viewtopic.php?f=15&t=3249
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Re: Acrolein in smoke suppresses the immune system

Postby DannyBoy » Mon May 17, 2010 8:41 pm

Thanks for that post. it is very useful.
DannyBoy
 
Posts: 2
Joined: Mon May 17, 2010 8:31 pm

Acrolein in smoke may cause M.S.

Postby Wilberforce » Thu Jun 16, 2011 12:03 pm

Findings suggest new cause, possible treatment for multiple sclerosis
November 23, 2010

note: image too large to display here
http://news.uns.purdue.edu/images/2010/shi-acrolein.jpg
This drawing depicts how the environmental pollutant acrolein may damage nerve insulation called myelin in multiple sclerosis. "A" represents the normal structure of nerve fibers and myelin; "B" represents how acrolein is thought to damage myelin and cell membranes; and "C" shows how nerves with damaged myelin cannot properly conduct signals. (Purdue University graphic/Michel Schweinsberg)

WEST LAFAYETTE, Ind. - Researchers have found evidence that an environmental pollutant may play an important role in causing multiple sclerosis and that a hypertension drug might be used to treat the disease.

The toxic substance acrolein was elevated by about 60 percent in the spinal cord tissues of mice with a disease similar to multiple sclerosis, said Riyi Shi, a medical doctor and a professor of neuroscience and biomedical engineering in Purdue University's Department of Basic Medical Sciences, School of Veterinary Medicine, Center for Paralysis Research and Weldon School of Biomedical Engineering.

The research results represent the first concrete laboratory evidence for a link between acrolein (pronounced a-KRO-le-an) and multiple sclerosis, he said.

"Only recently have researchers started to understand the details about what acrolein does to the human body," Shi said. "We are studying its effects on the central nervous system, both in trauma and degenerative diseases such as multiple sclerosis."

The toxic compound is found in air pollutants including tobacco smoke and auto exhaust. Acrolein also is produced within the body after nerve cells are damaged. Previous studies by this research team found that neuronal death caused by acrolein can be prevented by administering the drug hydralazine, an FDA-approved medication used to treat hypertension.

The new findings show that hydralazine also delays onset of multiple sclerosis in mice and reduces the severity of symptoms by neutralizing acrolein.

"The treatment did not cause any serious side effects in the mice," Shi said. "The dosage we used for hydralazine in animals is several times lower than the standard dosing for oral hydralazine in human pediatric patients. Therefore, considering the effectiveness of hydralazine at binding acrolein at such low concentrations, we expect that our study will lead to the development of new neuroprotective therapies for MS that could be rapidly translated into the clinic."

The researchers also learned the specific chemical signature of the drug that binds to acrolein and neutralizes it, potentially making it possible to create synthetic alternatives with reduced side effects. The studies are detailed in a paper appearing online this month in the journal Neuroscience. The paper was written by doctoral students Gary Leung, Wenjing Sun and Lingxing Zheng; graduate research assistant Melissa Tully, who is an MD-Ph.D. student at Purdue and the Indiana University School of Medicine; postdoctoral researcher Sarah Brookes; and Shi.

In multiple sclerosis, the myelin insulation surrounding nerve cells is destroyed and the nerve fibers themselves are damaged.

"We think that acrolein is what degrades myelin, so if we can block that effect then we can delay the onset of MS and lessen the symptoms," Shi said.

Acrolein induces the production of free radicals, compounds that cause additional injury to tissues after disease or physical trauma.

"We've discovered that acrolein may play a very important role in free radical injury, particularly in multiple sclerosis," Shi said.

The elevated acrolein levels in the MS mice were cut in half when treated with hydralazine. The drug represents a potential long-term therapy to slow the disease's progress.

"To our knowledge, this is the first evidence that acrolein acts as a neurotoxin in MS and also the first time anyone has demonstrated hydralazine to be a neuroprotective drug," Shi said.

Other researchers had previously shown that acrolein damages liver cells and that the damage can be alleviated by hydralazine, leading the Purdue researchers to study its possible effects on spinal cord tissues.

Further research will be conducted, and Shi's group has identified other potential compounds for binding acrolein. The research team, in a possible future collaboration with the Indiana University School of Medicine, also is working to improve the sensitivity of detection methods to measure acrolein levels in people with multiple sclerosis.

Writer: Emil Venere, 765-494-4709, venere@purdue.edu

Source: Riyi Shi, 765-496-3018, riyi@purdue.edu

Note to Journalists: A copy of the research paper is available from Emil Venere, Purdue News Service, at 765-494-4709, venere@purdue.edu.

source
http://www.evri.com/media/article;jsess ... title=Evri
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Re: Acrolein in smoke suppresses the immune system

Postby Wilberforce » Fri Jul 08, 2011 8:37 am

More on Acrolein, Wood Smoke and M.S.
viewtopic.php?f=11&t=3514
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Acrolein Decreases Endothelial Cell Migration and Insulin Se

Postby Wilberforce » Fri May 09, 2014 8:04 pm

http://toxsci.oxfordjournals.org/conten ... u087.short
Acrolein Decreases Endothelial Cell Migration and Insulin Sensitivity Through Induction of Let-7a

O'Toole, et al

Received March 7, 2014.
Accepted April 28, 2014.
Abstract

Acrolein is a major reactive component of vehicle exhaust, cigarette and wood smoke. It is also present in several food substances and is generated endogenously during inflammation and lipid peroxidation. Although previous studies have shown that dietary or inhalation exposure to acrolein results in endothelial activation, platelet activation and accelerated atherogenesis, the basis for these effects is unknown. Moreover, the effects of acrolein on microRNA (miRNA) have not been studied. Using AGILENT miRNA microarray high throughput technology, we found that treatment of cultured human umbilical vein endothelial cells with acrolein led to a significant (>1.5-fold) up-regulation of 12, and down-regulation of 15, miRNAs. Among the miRNAs up-regulated were members of the let-7 family and this up-regulation was associated with decreased expression of their protein targets, ß3 integrin, Cdc34 and K-Ras. Exposure to acrolein attenuated ß3 integrin-dependent migration and reduced Akt phosphorylation in response to insulin. These effects of acrolein on endothelial cell migration and insulin signaling were reversed by expression of a let-7a inhibitor. Also, inhalation exposure of mice to acrolein (1ppm x 6h/day x 4 days) up-regulated let-7a and led to a decrease in insulin-stimulated Akt phosphorylation in the aorta. These results suggest that acrolein exposure has broad effects on endothelial miRNA repertoire and that attenuation of endothelial cell migration and insulin signaling by acrolein is mediated in part by the up-regulation of let-7a. This mechanism may be significant feature of vascular injury caused by inflammation, oxidized lipids, and exposure to environmental pollutants.
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA

Acrolein and Asthma Attack Prevalence

Postby Wilberforce » Fri May 09, 2014 9:22 pm

http://www.plosone.org/article/info%3Ad ... ne.0096926
Acrolein and Asthma Attack Prevalence in a Representative Sample of the United States Adult Population 2000 – 2009

B. Rey deCastro

Published: May 09, 2014
DOI: 10.1371/journal.pone.0096926

Abstract
Background

Acrolein is an air toxic and highly potent respiratory irritant. There is little epidemiology available, but US EPA estimates that outdoor acrolein is responsible for about 75 percent of non-cancer respiratory health effects attributable to air toxics in the United States, based on the Agency's 2005 NATA (National-Scale Air Toxics Assessment) and acrolein's comparatively potent inhalation reference concentration of 0.02 µg/m3.
Objectives

Assess the association between estimated outdoor acrolein exposure and asthma attack reported by a representative cross-sectional sample of the adult United States population.
Methods

NATA 2005 chronic outdoor acrolein exposure estimates at the census tract were linked with residences oif adults (≥18 years old) in the NHIS (National Health Interview Survey) 2000 – 2009 (n = 271,348 subjects). A sample-weighted logistic regression model characterized the association between the prevalence of reporting at least one asthma attack in the 12 months prior to survey interview and quintiles of exposure to outdoor acrolein, controlling for potential confounders.
Results

In the highest quintile of outdoor acrolein exposure (0.05 – 0.46 µg/m3), there was a marginally significant increase in the asthma attack pOR (prevalence-odds ratio [95% CI] = 1.08 [0.98:1.19]) relative to the lowest quintile. The highest quintile was also associated with a marginally significant increase in prevalence-odds (1.13 [0.98:1.29]) in a model limited to never smokers (n = 153,820).
Conclusions

Chronic exposure to outdoor acrolein of 0.05 – 0.46 µg/m3 appears to increase the prevalence-odds of having at least one asthma attack in the previous year by 8 percent in a representative cross-sectional sample of the adult United States population.


"Important environmental triggers include ETS (environmental tobacco smoke), dust mites, cockroach allergen, outdoor air pollution, wood smoke, pets, and mold."

.
• The Surgeon General has determined that there is no safe level of exposure to ambient smoke!

• If you smell even a subtle odor of smoke, you are being exposed to poisonous and carcinogenic chemical compounds!

• Even a brief exposure to smoke raises blood pressure, (no matter what your state of health) and can cause blood clotting, stroke, or heart attack in vulnerable people. Even children experience elevated blood pressure when exposed to smoke!

• Since smoke drastically weakens the lungs' immune system, avoiding smoke is one of the best ways to prevent colds, flu, bronchitis, or risk of an even more serious respiratory illness, such as pneumonia or tuberculosis!
Does your child have the flu? Chances are they have been exposed to ambient smoke!
User avatar
Wilberforce
 
Posts: 5017
Joined: Wed Jul 25, 2007 11:36 pm
Location: USA


Return to Particle Pollution Research

Who is online

Users browsing this forum: No registered users and 1 guest