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Key Points

• Secondhand smoke (also called environmental tobacco smoke) is the combination of smoke given off by the burning end of a tobacco product and the smoke exhaled by the smoker (see Question 1).
• Of the chemicals identified in secondhand smoke, more than 50 have been found to cause cancer (see Question 3).
• Secondhand smoke causes lung cancer in nonsmokers (see Question 4).
• Secondhand smoke causes heart disease in adults and sudden infant death syndrome (SIDS), ear infections, and asthma attacks in children (see Question 5).
• There is no safe level of exposure to secondhand smoke (see Question 6).

The U.S. Surgeon General concluded back in 2006 that nearly 50,000 Americans die each year from secondhand smoke exposure. The findings of this new IOM report are significant, because they confirm that secondhand smoke exposure is a significant cause of acute coronary events, including heart attacks, and that there is no safe level of exposure. 

The report also concluded that relatively brief exposure to secondhand smoke can cause acute coronary events. It has already been shown that secondhand smoke also causes other serious diseases, including lung cancer.

This growing mountain of evidence makes it clear that secondhand smoke kills, and to protect the public health, smoking should be prohibited in all public areas and workplaces. The Lung Association’s Smokefree Air Challenge is dedicated to making this happen. 

To date, half of all states, along with the District of Columbia, have met our Smokefree Air Challenge by implementing comprehensive smokefree laws.  These laws protect all workers from toxic secondhand smoke in the workplace, and also protect customers from smoke in bars and restaurants, giving people with asthma and other lung diseases the freedom to dine and socialize wherever they choose.

Now with even more evidence of the dangers of secondhand smoke from this new report, it is time for the remaining 25 states to protect their citizens by meeting our Smokefree Air Challenge and joining the American Lung Association in our fight to save lives by improving lung health and preventing lung disease.

To learn more about the American Lung Association’s Smokefree Air Challenge, please visit www.lungusa.org/smokefree.

Secondhand smoke exposure causes disease and premature death in children and adults who do not smoke.  Secondhand smoke contains hundreds of chemicals known to be toxic or carcinogenic, including formaldehyde, benzene, vinyl chloride, arsenic, ammonia and hydrogen cyanide.

Secondhand smoke causes about 50,000 deaths in adult nonsmokers in the United States each year, including approximately 3,400 from lung cancer and up to 69,600 from heart disease.

Secondhand smoke is esecially harmful to young children.  Secondhand smoke is responsible for between 150,000 and 300,000 lower respiratory tract infections in infants and children under 18 months of age.

In the United States, 25 million, or 35 percent of, children live in homes where residents or visitors smoke in the home on a regular basis.  Approximately 50-75 percent of children in the United States have detectable levels of cotinine, the breakdown product of nicotine in their blood.

Reference:
American Lung Association (2009) Confirmed – secondhand smoke causes heart attacks.  Retrieved November 1, 2009 from http://www.lungusa.org/about-us/our-impact/top-stories/secondhand-smoke-heart-attacks.html

Insulin, folate metabolism influence circadian rhythms, according to Penn studyPHILADELPHIA – While scientists have known for several years that our body’s internal clock helps regulate many biological processes, researchers have found that the reverse is also true: Many common biological processes – including insulin metabolism – regulate the clock, according to a new study by investigators at the University of Pennsylvania School of Medicine, the Genomics Institute of the Novartis Research Foundation, and the University of California at San Diego.

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  The Expanded Clock Gene Network. (Click to view larger version.)

Related Links

• BioGPS Database
• BioGPS Circadian Gene Data
• A Biological Basis for the 8-Hour Workday?
• Institute for Translational Medicine and Therapeutics
• University of Pennsylvania School of Medicine
• University of Pennsylvania Health System

The new data, published online in Cell this week, suggest that someday physicians may be able to use small molecules that inhibit or stimulate these biological processes in order to influence a person’s clock when it gets out of sync due to jetlag or shift work. Researchers may also be able to find new ways to treat metabolic disorders that are intimately tied to the body’s daily cycles.

Using a genome-wide screen, the investigators found that reducing expression of any one of hundreds of genes could substantially alter the length of the circadian cycle, which controls the 24-hour sleep/wake cycle. The clock-influencing genes are involved in a large number of biological processes, but the researchers found that components of insulin metabolism, folate metabolism, and the cell cycle were overrepresented in the gene screen, suggesting that these pathways are closely linked to the clock.

“Clock biologists all appreciated that the communication went one direction – from the clock to biological processes – but I don’t think anyone anticipated that there would be this level of integration with cell metabolism and the cell cycle, or all these other pathways impinging on clock function,” says John Hogenesch, PhD, Associate Professor of Pharmacology in the Institute for Translational Medicine and Therapeutics at Penn. Hogenesch is a co-senior author on the paper with Steve Kay, Dean of the Division of Biological Sciences at UCSD. “There were some hints this might occur for some genes, but not to this extent.”

The idea that biological processes might have feedback systems with the circadian clock makes some sense to Hogenesch. For example, he points to the influence of insulin metabolism, saying “If your energy requirements aren’t being met, instead of spending a lot of energy on a cell division, a cell might necessarily delay it. It is the same strategy we use when we are not ready to do something, we delay. Maybe procrastination is an evolutionary cellular strategy enabled by the clock to confront situations where resources are limited.”

While biologists regularly draw molecular pathways as if they are distinct from one another, they know the reality is much different. “This is a good example showing how dozens of pathways are functionally interconnected with clock function and vice versa,” Hogenesch says. “It is important to remember that when you start to change function with a drug, for example, that the perturbation can have unanticipated consequence. Sometimes these consequences are good, but sometimes not.”

Hogenesch stresses that while the new experiments show a feedback loop between biological processes and the clock in individual cells in culture, it is not yet clear how feedback systems work in the whole organism. Currently the team is working on biochemical and genetic experiments to answer that question.

In addition to publishing the data in the journal, the investigators have displayed the data on the BioGPS open-access searchable database (http://biogps.gnf.org). The circadian genome-wide screen data can be found at http://biogps.gnf.org/circadian/ and are linked to expression data from Penn, gene function data at Wikipedia and the National Center for Biotechnology Information (NCBI), as well as gene structure information from the University of California at Santa Cruz.

Hogenesch, who helped develop the website when he worked at the Genomics Institute of the Novartis Research Foundation in San Diego, said the site relies on web 2.0 technology and is very simple to use and customize. He and his colleagues built the site because many researchers want to do large database searches but are not computer scientists or informatics specialists. “Andy Su [of Novartis] and I decided to develop a site that even my mom could use, and pitched at the 90 percent of biologists who want to use something but don’t have the skill sets. We decided to build something that would allow them to take advantage of large datasets such as this one.”

Co-first authors on the paper are Eric E. Zhang and Tsuyoshi Hirota of the Genomics Institute of the Novartis Research Foundation, and UCSD, and Andrew C. Liu, of the Genomics Institute of the Novartis Research Foundation and the University of Memphis, Tenn. Other authors on the paper include Loren J. Miraglia, Genevieve Welch, Xianzhong Liu, Jon W. Huss III, Jeff Janes, and Andrew I. Su of the Genomics Institute of the Novartis Research Foundation, and Pagkapol Y. Pongsawakul, Ann Atwood, and Steve A. Kay of UCSD.

This research was funded by Silvio O. Conte Center and the National Institute of Mental Health. 

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PENN Medicine is a $3.6 billion enterprise dedicated to the related missions of medical education, biomedical research, and excellence in patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation’s first medical school) and the University of Pennsylvania Health System.

Penn’s School of Medicine is currently ranked #3 in the nation in U.S.News & World Report’s survey of top research-oriented medical schools; and, according to the National Institutes of Health, received over $366 million in NIH grants (excluding contracts) in the 2008 fiscal year. Supporting 1,700 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

The University of Pennsylvania Health System (UPHS) includes its flagship hospital, the Hospital of the University of Pennsylvania, rated one of the nation’s top ten “Honor Roll” hospitals by U.S.News & World Report; Pennsylvania Hospital, the nation’s first hospital; and Penn Presbyterian Medical Center, named one of the nation’s “100 Top Hospitals” for cardiovascular care by Thomson Reuters. In addition UPHS includes a primary-care provider network; a faculty practice plan; home care, hospice, and nursing home; three multispecialty satellite facilities; as well as the Penn Medicine at Rittenhouse campus, which offers comprehensive inpatient rehabilitation facilities and outpatient services in multiple specialties.