| ACAS Projects: Smoke-Free Casinos | Teens And Tobacco | Smoke-Free Multi-Unit Housing | Education And Reference | Smoke-Free Foster Homes |
As public awareness of
commercial tobacco's
deadly effects has
grown, so has the
tobacco consumer's
desire to quit the
products increased. The
tobacco industry has
answered this threat to
its bottom line by
increasing the amounts
of the addictive agent
nicotine in tobacco
products, making it more
difficult for those
tobacco-users to quit.
commercial tobacco's
deadly effects has
grown, so has the
tobacco consumer's
desire to quit the
products increased. The
tobacco industry has
answered this threat to
its bottom line by
increasing the amounts
of the addictive agent
nicotine in tobacco
products, making it more
difficult for those
tobacco-users to quit.
| More info these locations: http://eetd.lbl.gov/IED/symposium-07/pdf/ied-symposium-07-singer.pdf http://www.lbl.gov/ Lawrence Berkeley National Laboratory |
| Brett C. Singer & Hugo Destaillats, Indoor Environment Department Lawrence Berkeley National Laboratory |
Education & Reference:
525 W Southern Ave. Suite #110 Mesa, AZ 85210 | ph: 480.733.5864 | fax: 480.733.1844 | smokefreeaz@yahoo.com
An estimated 50 to 75 percent (280,000 to 425,000) of all cancer deaths are caused by human
behaviors, such as smoking, eating unhealthy foods, and not getting regular exercise, according to the
National Cancer Institute (NCI).
Avoiding tobacco use is the single most important step you can take to reduce your cancer risk.
Tobacco use causes about 30 percent (169,000) of all cancer deaths in the United States each year.
Cigarette smoking is responsible for almost all cases of lung cancer. It also is linked to cancers of the
mouth, larynx, esophagus, stomach, pancreas, kidney and bladder. Pipe smoke, cigars, and smokeless
tobacco also can cause cancer.
Another one-third of all cancer deaths are thought to be caused by a poor diet. The exact links between
diet and cancer remain unclear. However, researchers have found that a diet high in fat increases our
risk for cancer, especially colon cancer. On the other hand, a low-fat diet that includes lots of fruits,
vegetables, and whole grains appears to lower our cancer risk.
Not being physically active has been associated with the development of several types of cancer.
Regular exercise may reduce our risk of colon cancer by 50 percent, and it may also lower the risk of
cancers of the breast and prostate.
behaviors, such as smoking, eating unhealthy foods, and not getting regular exercise, according to the
National Cancer Institute (NCI).
Avoiding tobacco use is the single most important step you can take to reduce your cancer risk.
Tobacco use causes about 30 percent (169,000) of all cancer deaths in the United States each year.
Cigarette smoking is responsible for almost all cases of lung cancer. It also is linked to cancers of the
mouth, larynx, esophagus, stomach, pancreas, kidney and bladder. Pipe smoke, cigars, and smokeless
tobacco also can cause cancer.
Another one-third of all cancer deaths are thought to be caused by a poor diet. The exact links between
diet and cancer remain unclear. However, researchers have found that a diet high in fat increases our
risk for cancer, especially colon cancer. On the other hand, a low-fat diet that includes lots of fruits,
vegetables, and whole grains appears to lower our cancer risk.
Not being physically active has been associated with the development of several types of cancer.
Regular exercise may reduce our risk of colon cancer by 50 percent, and it may also lower the risk of
cancers of the breast and prostate.
Thanks to: UCSF Helen Diller Family Comprehensive Cancer Center
How many cancer deaths are attributed to lifestyle choices?
World Headlines
ACAS/ArizonaHeadlines
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Officers
Projects
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Health Links
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ACAS/ArizonaHeadlines
Smoke-Free AZ History
Officers
Projects
Mark Your Calendar
Napolitano Honored
Health Links
Volunteers Slideshow
Contact Us
Consequences of dramatic reductions in state tobacco control funds: Florida, 1998–2000
Published Online First: 7 April 2008. doi:10.1136/tc.2007.024331 Tobacco Control 2008;17:205-210
| http://tobaccocontrol.bmj.com/ RESEARCH PAPERS |
J Niederdeppe1, M C Farrelly2, J C Hersey3, K C Davis2
1 Department of Population Health Sciences and Center for Tobacco Research and Intervention,
University of Wisconsin, Madison, Wisconsin, USA
2 Public Health Research programme and Center of Excellence in Health Promotion Economics, RTI
International, North Carolina, USA
3 RTI International, Washington, DC, USA
Correspondence to:
J Niederdeppe, Department of Population Health Sciences and Center for Tobacco Research and
Intervention, University of Wisconsin, 610 Walnut Street, Room 707 WARF Building, Madison, WI
53726-2397, USA; niederdeppe@wisc.edu
Objective: This study assessed whether dramatic funding reductions to the Florida Tobacco Control
Program (FTCP) influenced trends in recall of the Florida "truth" anti-smoking media campaign,
anti-industry attitudes and non-smoking intentions among Florida teens.
Methods: We used an interrupted time series technique to test for differences in the rates of change in
Florida "truth" recall, anti-industry beliefs and non-smoking intentions before and after the FTCP budget
cuts using the Florida Anti-tobacco Media Evaluation (FAME) survey, a repeated cross-sectional
telephone survey of Florida teens.
Results: Recall of the Florida "truth" anti-smoking campaign, anti-industry attitudes, and non-smoking
intentions increased dramatically between April 1998 and May 1999. Florida "truth" recall declined after
FTCP budget cuts in June 1999. Anti-industry beliefs and non-smoking intentions plateaued or began to
decline after the budget cuts. The launch of the national "truth" campaign in February 2000 may have
offset otherwise deleterious effects of the budget cuts on anti-industry beliefs, but not smoking
intentions.
Conclusion: Reductions in tobacco control funding have immediate effects on programme exposure
and cognitive precursors to smoking initiation. There is a critical need to maintain and enhance funding
for state tobacco control programmes to continue nationwide progress in preventing youth from initiating
cigarette smoking.
1 Department of Population Health Sciences and Center for Tobacco Research and Intervention,
University of Wisconsin, Madison, Wisconsin, USA
2 Public Health Research programme and Center of Excellence in Health Promotion Economics, RTI
International, North Carolina, USA
3 RTI International, Washington, DC, USA
Correspondence to:
J Niederdeppe, Department of Population Health Sciences and Center for Tobacco Research and
Intervention, University of Wisconsin, 610 Walnut Street, Room 707 WARF Building, Madison, WI
53726-2397, USA; niederdeppe@wisc.edu
Objective: This study assessed whether dramatic funding reductions to the Florida Tobacco Control
Program (FTCP) influenced trends in recall of the Florida "truth" anti-smoking media campaign,
anti-industry attitudes and non-smoking intentions among Florida teens.
Methods: We used an interrupted time series technique to test for differences in the rates of change in
Florida "truth" recall, anti-industry beliefs and non-smoking intentions before and after the FTCP budget
cuts using the Florida Anti-tobacco Media Evaluation (FAME) survey, a repeated cross-sectional
telephone survey of Florida teens.
Results: Recall of the Florida "truth" anti-smoking campaign, anti-industry attitudes, and non-smoking
intentions increased dramatically between April 1998 and May 1999. Florida "truth" recall declined after
FTCP budget cuts in June 1999. Anti-industry beliefs and non-smoking intentions plateaued or began to
decline after the budget cuts. The launch of the national "truth" campaign in February 2000 may have
offset otherwise deleterious effects of the budget cuts on anti-industry beliefs, but not smoking
intentions.
Conclusion: Reductions in tobacco control funding have immediate effects on programme exposure
and cognitive precursors to smoking initiation. There is a critical need to maintain and enhance funding
for state tobacco control programmes to continue nationwide progress in preventing youth from initiating
cigarette smoking.
Thanks to: Karen Zielaski, Project Director, Healthy Policies, E-mail: healthypolicies@earthlink.net Office: 1(520)290-0032
Ever wonder if there is a health risk just being in a room reeking with the smell of tobacco smoke?
Apparently, the answer is "yes"!
Nicotine in secondhand tobacco smoke (SHS) reacts differently than most SHS particles in that it collects
rapidly on environmental surfaces, especially cotton and wallboard. This process quickly reduces the
concentration in the air while it increases the layer "sorbed" on carpeting, bedding, furniture, walls, etc.
Over time the amount of cotinine, nicotine's byproduct, on these surfaces can greatly exceed the
amount in the air, even in a smoke-filled room.
This sorbed nicotine reacts with the ozone in our air through a process called desorption. Since Ozone
exists in increasing amounts in our cities due to the reaction of sunlight with hydrocarbon pollution from
vehicles, paint, oil and chemical plants, etc. so desorption is a constant process. Nicotine
desorptionreleases nicotinaldehyde, myosmine, cotinine (nicotine by-product), Nmethylformamide (an
organic solvent) , formaldehyde (regulated as a carcinogen) and other chemicals.
In areas of heavy nicotine deposits, smoking rooms in hotels, "private" clubs, smoking bars and
smoker's homes, desorption rates can equal the rates of nicotine oxidation during actual smoking.
Smoking inside a room already heavy with the "odor" of tobacco greatly increases the risk for the
smoker, and creates a risk for all who enter the room long after the smoke appears to have dissipated.
Substantial levels of airborne and surface nicotine have been measured in the homes of smokers who
had previously ceased smoking indoors.
Some researchers fear that third hand smoke may be far more dangerous than previously realized. In
addition to the obvious health risk to the housekeeping employees and other helpers cleaning the
smoking rooms in motels and restaurants, this is a problem for the employees and patrons of “private”
clubs and other places that usually allow smoking, but later claim they are now smokefree when they
invite people in, including children, in for smokefree events.
Apparently, the answer is "yes"!
Nicotine in secondhand tobacco smoke (SHS) reacts differently than most SHS particles in that it collects
rapidly on environmental surfaces, especially cotton and wallboard. This process quickly reduces the
concentration in the air while it increases the layer "sorbed" on carpeting, bedding, furniture, walls, etc.
Over time the amount of cotinine, nicotine's byproduct, on these surfaces can greatly exceed the
amount in the air, even in a smoke-filled room.
This sorbed nicotine reacts with the ozone in our air through a process called desorption. Since Ozone
exists in increasing amounts in our cities due to the reaction of sunlight with hydrocarbon pollution from
vehicles, paint, oil and chemical plants, etc. so desorption is a constant process. Nicotine
desorptionreleases nicotinaldehyde, myosmine, cotinine (nicotine by-product), Nmethylformamide (an
organic solvent) , formaldehyde (regulated as a carcinogen) and other chemicals.
In areas of heavy nicotine deposits, smoking rooms in hotels, "private" clubs, smoking bars and
smoker's homes, desorption rates can equal the rates of nicotine oxidation during actual smoking.
Smoking inside a room already heavy with the "odor" of tobacco greatly increases the risk for the
smoker, and creates a risk for all who enter the room long after the smoke appears to have dissipated.
Substantial levels of airborne and surface nicotine have been measured in the homes of smokers who
had previously ceased smoking indoors.
Some researchers fear that third hand smoke may be far more dangerous than previously realized. In
addition to the obvious health risk to the housekeeping employees and other helpers cleaning the
smoking rooms in motels and restaurants, this is a problem for the employees and patrons of “private”
clubs and other places that usually allow smoking, but later claim they are now smokefree when they
invite people in, including children, in for smokefree events.
Third Hand Smoke: Is It A Threat To Your Health?
| By: R Johnson, ACAS Webmaster |
| For more information see, http://cancerweb.ncl .ac.uk/ http://www.epa.gov/iaq/voc.html http://whyfiles.org/030air_pollution/ozone1.html http://www.public.asu.edu/~hdestail/research.htm#3 |
| Our Purpose Is To Save Lives |
Tear cytokine and ocular surface alterations following brief passive cigarette smoke
exposure
exposure
| Cytokine. 2008 Jul 2. |
| Rummenie VT, Matsumoto Y, Dogru M, Wang Y, Hu Y, Ward SK, Igarashi A, Wakamatsu T, Ibrahim O, Goto E, Luyten G, Inoue H, Saito I, Shimazaki J, Tsubota K. Keio University School of Medicine, Johnson & Johnson Ocular Surface and Visual Optics Department, Shinanomachi 35, Shinjuku-ku, Tokyo, Japan; Keio University School of Medicine, Department of Ophthalmology, Tokyo, Japan; Erasmus University School of Medicine, Department of Ophthalmology, Rotterdam, The Netherlands. Abstract |
Purpose: To prospectively investigate the effects of acute passive cigarette smoke exposure on the
ocular surface and tear film in healthy non-smokers.
Methods: Twelve right eyes of 12 subjects without any ocular diseases were examined before, 5min,
and 24h after 5min of passive cigarette smoke exposure in a controlled smoke chamber. Tear samples
were obtained before, 5min and 24h after smoke exposure to detect tear hexanoyl-lysine (HEL), acrolein
and inflammatory cytokine concentrations. Tear evaporation rate, DR-1 tear film lipid layer
interferometry, tear film break-up time (TBUT), ocular surface fluorescein staining (FS) and Rose Bengal
staining (RB), Schirmer I test were performed before, 5min, and 24h after smoke exposure. Conjunctival
impression cytology (IC) and brush cytology (BC) were carried out before and 24h after smoke exposure.
Results: Tear evaporation rate, tear lipid spread time, tear film break-up time, and vital staining scores
showed significant worsening with passive smoke exposure. Tear HEL and IL-6 concentrations
increased significantly 24h after smoke exposure. Tear acrolein level showed an insignificant increase at
5min. IC and RT-PCR revealed a significant reduction in goblet cell density, a shift toward higher
squamous metaplasia grades and a significant downregulation of MUC5AC mRNA expression at 24h.
Conclusion: Even brief passive exposure to cigarette smoke in healthy non-smoker subjects was
associated with adverse effects on the ocular surface health as evidenced by an increase of tear
inflammatory cytokines, tear lipid peroxidation products and decrease of mucosal defense resulting in
tear instability and damage to the ocular surface epithelia.
ocular surface and tear film in healthy non-smokers.
Methods: Twelve right eyes of 12 subjects without any ocular diseases were examined before, 5min,
and 24h after 5min of passive cigarette smoke exposure in a controlled smoke chamber. Tear samples
were obtained before, 5min and 24h after smoke exposure to detect tear hexanoyl-lysine (HEL), acrolein
and inflammatory cytokine concentrations. Tear evaporation rate, DR-1 tear film lipid layer
interferometry, tear film break-up time (TBUT), ocular surface fluorescein staining (FS) and Rose Bengal
staining (RB), Schirmer I test were performed before, 5min, and 24h after smoke exposure. Conjunctival
impression cytology (IC) and brush cytology (BC) were carried out before and 24h after smoke exposure.
Results: Tear evaporation rate, tear lipid spread time, tear film break-up time, and vital staining scores
showed significant worsening with passive smoke exposure. Tear HEL and IL-6 concentrations
increased significantly 24h after smoke exposure. Tear acrolein level showed an insignificant increase at
5min. IC and RT-PCR revealed a significant reduction in goblet cell density, a shift toward higher
squamous metaplasia grades and a significant downregulation of MUC5AC mRNA expression at 24h.
Conclusion: Even brief passive exposure to cigarette smoke in healthy non-smoker subjects was
associated with adverse effects on the ocular surface health as evidenced by an increase of tear
inflammatory cytokines, tear lipid peroxidation products and decrease of mucosal defense resulting in
tear instability and damage to the ocular surface epithelia.
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WDF-4SWXDGR-1&_user=10&_coverDate=07%2F03%2F2008&_alid=7
73303243&_rdoc=1&_fmt=high&_orig=search&_cdi=6765&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000050221&_version=1&_ur
lVersion=0&_userid=10&md5=2b83ebc15b4f55d0b28234432ecd6ed6
73303243&_rdoc=1&_fmt=high&_orig=search&_cdi=6765&_sort=d&_docanchor=&view=c&_ct=2&_acct=C000050221&_version=1&_ur
lVersion=0&_userid=10&md5=2b83ebc15b4f55d0b28234432ecd6ed6
Receive timely E-mail Updates On Tobacco Control Issues. Sign up and receive information about tobacco policy and advocacy.
Contact Karen Zielaski for information regarding support for her services: healthypolicies@earthlink.net Tel 520: 290-0032
Contact Karen Zielaski for information regarding support for her services: healthypolicies@earthlink.net Tel 520: 290-0032
| View excellent informational Flash presentation on Tobacco Smoke and Lung Cancer, created by MSNBC with information provided by the Mayo Clinic. Click graphic above. |
| For technical issues or errors: webmasterACAS@cox.net | Rick Johnson |
Thanks to: Karen Zielaski, Project Director, Healthy Policies, E-mail: healthypolicies@earthlink.net Office: 1(520)290-0032
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