вторник, 18 декабря 2007 г.

Radon

What Is Radon?

Radon-222 is a colorless, odorless, radioactive gas. It forms from the decay of naturally occurring uranium-238, which is found in soil and rock throughout the world. Radon is present both outdoors and indoors. Exposure in homes mostly results from radon-contaminated gas rising from the soil. This makes it an unusual indoor air pollutant in that it has a natural source. Exposure to radon is also a known cause of lung cancer in underground miners of uranium and other ores. Thus, its presence in indoor air has raised concern that it may also be a cause of lung cancer for the entire population.

Radon has a half-life of 3.8 days; that is, half of a given amount takes 3.8 days to decay. It breaks down into a series of solid elements called radon progeny. Several of these elements (such as polonium-218, polonium-214, and lead-214) emit radiation in the form of alpha particles. An alpha particle consists of 2 protons and 2 neutrons, like the nucleus of a helium atom, and carries a positive charge. Although alpha particles do not penetrate deeply into tissue (as gamma radiation can), they carry enough energy to permanently change DNA if they reach the nucleus of a cell. As a result, when inhaled radon progeny reach the lungs, the alpha particles can damage cells within the airways and thereby increase lung cancer risk.

How Are People Exposed to Radon?

A link between cancer and working in underground mines was suspected even before radon was identified as an element. In 1556, German scholar Georgius Agricola wrote in De re metallica about the high death rates of miners in the Carpathian Mountains of Eastern Europe. More than 300 years later, autopsy studies of miners in that region revealed a common cause of death to be chest tumors, which were later shown to be primary lung cancer.

In the early 20th century, high levels of radon were found in mines in Germany and Czechoslovakia (now the Czech Republic), and researchers believed that this exposure led to the miners’ lung cancer. In the 1950s, radiation scientists recognized that tiny particles of radon progeny and not radon gas delivered the radiation dose that caused the cancer. Epidemiologic studies of radon-exposed miners during the 1950s and 1960s confirmed the connection between radon exposure and lung cancer (NRC, 1998).

A recent concern is whether radon exposure might also cause lung cancer in the general population. Adults and children are exposed to radon in homes, commercial buildings, schools, and other places. The radon gas emitted by soil or rock enters the buildings through cracks in floors or walls; construction joints; or gaps in foundations around pipes, wires, or pumps. Without ventilation or another way of dissipating, radon can build up and reach rather high levels.

Within buildings, radon levels are usually highest in the basement. This level is closest to the soil from which the radon-containing gas diffuses. Therefore, people who spend much of their time in basement rooms at home or at work would have a greater risk for exposure.

Radon emitted into outdoor spaces generally disperses and does not reach high levels. Indoor exposure is usually far lower than the occupational exposure for miners. However, the range of levels in the most contaminated homes approaches levels found in mines and may exceed the exposure standards permitted for underground miners.

Radon levels in the air are measured by units of radioactivity per volume of air. The most common concentration measure used is picocuries per liter (pCi/L). Background outdoor levels of radon range from near 0 to over 2 pCi/L. The US Environmental Protection Agency (EPA) has set an action level of 4 pCi/L as an annual average for homes and schools, and the National Council of Radiation Protection recommends a limit of no more than 8 pCi/L indoors.

Radon concentration may also be expressed in units of becquerels per cubic meter (Bq/m3) or as a working level (WL), a unit applied previously to underground mines. Exposure to radon or radon progeny incorporates the time spent at different concentrations; one commonly used unit for exposure is the working level month, which refers to spending 1 working month of time at a concentration of 1 WL.

The level of personal exposure to radon varies, depending on the concentration at home and any occupational exposure. Higher levels of radon exposure are more likely for people who:

* work in some underground mines (not only uranium but also some other types), in caves, or in uranium processing factories
* come in contact with phosphate fertilizers, which have high levels of radium (the immediate precursor of radon)
* live near uranium mines, although few facilities are now operating

Radon exposure can occur through drinking water, but this type of exposure is minimal. As the radon moves from the water to air, it can be inhaled. Water that comes from deep, underground wells in rock with high radium concentrations may have high levels of radon, whereas surface water (drawn from lakes or rivers) usually has very low radon levels. For the most part, water does not contribute much to the overall exposure to radon.

Radon exposure can also occur from some building materials if they are made from radon-containing substances. Specific instances of higher levels have been linked to particular building materials. For example, in Sweden, wallboard made with phosphogypsum having a high concentration of radium led to elevated concentrations of radon. Such materials usually contribute significantly to radon exposure.

The potential of the soil to release radon and contaminate homes depends on the concentration of radium and the characteristics of the earth. As a result, radon levels vary greatly in different parts of the United States, even within small geographic regions. As shown by the US Geological Survey map (see Figure), an area in the mid-Atlantic states stretching from New York through Pennsylvania to Maryland and Virginia, as well as a broad stretch of the upper Midwest, has geological formations that yield higher radon levels. In contrast, radon levels are low in the Southeast as far west as Texas and along much of the West coast. However, elevated radon levels have been found in almost every state.

The EPA estimates that as many as 8 million homes in the United States have elevated radon levels (EPA, 1998). The EPA posts detailed geographic information on radon levels, including state maps, on its Web site at www.epa.gov/iaq/radon/zonemap.html. The US Geological Survey publishes a series of geologic radon potential books that provide detailed geographic information, also available at energy.cr.usgs.gov/radon/radonhome.html

Does Radon Cause Cancer?

Radon is among the best studied of environmental carcinogens. Through epidemiologic, animal, and laboratory studies, we’ve come to understand how inhaling radon progeny can deliver a radiation dose to the lungs and how alpha particles emitted by radon progeny can damage the cells. We’ve also learned more about the degree of lung cancer risk associated with radon exposure. This evidence is summarized in Health Effects of Exposure to Radon, the 1998 report of the National Research Council’s Committee on the Biological Effects of Ionizing Radiation (BEIR) VI, often called the BEIR VI report.

What Do Epidemiologic Studies Show?

The epidemiologic evidence on radon and lung cancer risk comes from (1) cohort studies of underground miners with rather high levels of radon exposure, (2) case-control studies that compare radon exposure of persons with lung cancer and appropriate controls from the general population, and (3) ecologic studies comparing lung cancer deaths or incidence across geographic areas with differing levels of radon exposure. The cohort studies provided the first evidence showing that radon is a cause of lung cancer. These studies have also been used for estimating the risk of radon exposure. Once the problem of indoor radon was widely recognized, the case-control and ecologic studies were initiated.

Scientists have studied many groups of underground miners exposed to radon, including uranium miners in Czechoslovakia, France, Canada, Australia, and the US; fluorspar miners in Canada; iron miners in Sweden; and tin miners in China. To estimate lung cancer risk, researchers gathered data from 11 cohort studies, including 68,000 miners with 2,700 deaths from lung cancer. They looked at how lung cancer risk varies with exposure to radon and other factors, including cigarette smoking. At all but the highest levels, risk increases as exposure increases. In those miners known to be nonsmokers, a direct relationship between lung cancer risk and exposure also exists. These studies of miners provide good information on the relationship between increasing radon exposure and lung cancer risk at high levels of exposure.

However, average radon concentrations in the indoor air of most homes are considerably lower than those in uranium mines. The EPA set recommended levels for maximum concentration of radon in homes based on extrapolation from high occupational exposures to the generally much lower residential exposures. Researchers have subsequently confirmed the reliability of these risk estimates by combining the results of multiple studies of indoor radon exposures. The observed risk of lung cancer from indoor radon exposures approximates that which was predicted by studies of uranium miners exposed at much higher doses.

In 1998, the Biological Effects of Ionizing Radiation (BEIR VI) Committee of the National Research Council estimated that between 10% and 14% of lung cancer deaths in the US could be attributed to radon. Most of the radon-related lung cancers occur among smokers. However, an estimated 2,100-2,900 of the 11,000 deaths from lung cancer among nonsmokers in the United States each year are estimated to be radon-related.

What Do Animal and Laboratory Studies Suggest?

Like the studies done with miners, experimental studies on animals have clearly shown a risk of lung cancer with exposure to radon. These animal studies revealed that breathing in radon and its progeny (chemical products of radon decay) significantly increased the incidence of respiratory tract tumors. Nonspecific effects on the lungs have also been reported. In laboratory studies using human cells, radon and its decay products induced chromosomal abnormalities and other signs of permanent cellular change.

What Do the Experts Say?

The National Toxicology Program (NTP) evaluates exposures that may be carcinogenic. Exposures that are thought to cause cancer are included in the Reports on Carcinogens, published every 2 years. Each exposure is assigned to 1 of 2 categories: "known to be human carcinogens" or "reasonably anticipated to be human carcinogens." The first category includes substances for which human studies (epidemiologic studies or experimental studies) provide "sufficient evidence" of carcinogenicity in humans. The second category includes substances for which there is limited evidence of carcinogenicity in humans or sufficient evidence of carcinogenicity in experimental animals. Using this scheme, the NTP classifies radon as a "known human carcinogen.”

The International Agency for Research on Cancer (IARC) also evaluates exposures that may be carcinogenic. IARC classifies exposures into 1 of 4 categories:

* Group 1 exposures are those "known to be carcinogenic to humans," usually based on "sufficient" human evidence but sometimes based on "sufficient" evidence in experimental animals and "strong" human evidence.

* Group 2 exposures are divided into 2 categories; Group 2A ("probably carcinogenic to humans") has stronger evidence, and Group 2B ("possibly carcinogenic to humans") has weaker evidence.

* Group 3 exposures are not considered classifiable because available evidence is limited or inadequate.

* Group 4 exposures are "probably not carcinogenic to humans," based on evidence suggesting lack of carcinogenicity in humans and in experimental animals.

IARC rates radon as "carcinogenic to humans" (Group 1).

The Environmental Protection Agency (EPA), through its Integrated Risk Information System, uses a classification scheme similar to that of IARC. It classifies exposures into 1 of 5 categories:

* (A) human carcinogen
* (B) probable human carcinogen
* (C) possible human carcinogen
* (D) not classifiable as to human carcinogenicity
* (E) evidence of noncarcinogenicity for humans

The EPA has not classified radon as to its carcinogenicity.

The Agency for Toxic Substances and Disease Registry (ATSDR) has concluded that radon is carcinogenic.

Does Radon Cause Any Other Health Problems?

There is convincing evidence that radon causes lung cancer. Some studies of miners further suggest a connection between radon exposure and nonmalignant (non-cancerous) respiratory disease, especially pulmonary fibrosis (scar tissue formation in the lungs that leads to shortness of breath). These effects appear primarily in miners with high levels of exposure. The patterns seen on radiographs are not typical of silicosis (a lung disease caused by overexposure to crystalline silica), which is also a problem in the uranium miners.

Some evidence has also linked radon exposure with malignancies other than lung cancer. An analysis of the 11 cohort studies of miners found an increase in leukemia and in cancers of the stomach and liver. Risk for these cancers in the miners does not increase with the level of exposure, and these associations do not appear to be causal. Ecologic studies have linked radon with elevations of cancers other than lung cancer but without any consistent pattern. A recent case-control study of acute lymphocytic leukemia did not show an increased risk linked to radon exposure. Because radon is absorbed mainly through inhalation, and because alpha particles penetrate tissues only superficially, effects on tissues other than lung tissue would not be expected.

What Should I Do If I’ve Been Exposed to Radon?

Concerned patients may ask their doctor about medical tests for radon exposure. At present, no test is sensitive enough to determine past levels of exposure. Researchers are evaluating some methods for estimating past exposure (for example, special counting of levels of radiation in the skull), but these lack the needed sensitivity for most exposures in the general population.

For people exposed to higher levels of radon, it is especially important to quit smoking. Evidence has shown that the combined effect of cigarette smoking and radon exposure can cause lung cancer. For miners, the synergy between smoking and radon exposure has resulted in extremely high health risks.

For those miners whose health was compromised by exposure to radon, the United States has established a national compensation approach through the Radiation Exposure Compensation Act, passed in 1990 (Radiation Exposure Compensation Act Committee) and amended in 2000. The act began with an apology to the uranium miners and offered compensation to miners for lung cancer and selected nonmalignant lung diseases, if selected criteria were met. Health care professionals should be aware of the availability of this compensation for eligible persons.

How Can I Avoid Exposure to Radon?

Radon exposure in homes can be assessed readily. You can purchase radon detection kits in hardware or home supply stores. Some common types of detectors include charcoal canisters, alpha track devices, electret ion chambers, continuous monitors, and charcoal liquid scintillation detectors. Do-it-yourself kits are placed in the home for several days or for as long as 3 months and then mailed to a laboratory for analysis. Alternatively, you can hire private contractors to perform this testing. Qualified contractors can be located through state radon offices, which are listed on the EPA web site at www.epa.gov/iaq/contacts.html.

The EPA recommends remediation if test results show radon levels above 4 pCi/L. This value refers to the annual average, and the short-term tests often used at the time of sale of a home tend to give measurements that are biased upward from the actual value if the EPA protocol is followed. If values exceed the guideline, you should perform a repeat measurement, generally using one of the longer-term devices if possible.

Remediation can be performed by the homeowner, depending on the approach, or by a commercial contractor. A variety of methods can be used to reduce radon levels in your home, such as sealing cracks in floors and walls or increasing ventilation through "sub-slab depressurization" using pipes and fans. Again, qualified contractors can be located through state radon offices, which are listed on the EPA web site at www.epa.gov/iaq/contacts.html.

Certain building materials may be more "radon tight" and may help reduce exposure in areas where radon levels are high. You can obtain further information from state radon offices or from qualified contractors.

The Bottom Line

Radon is a naturally occurring environmental carcinogen. It is estimated that radon exposure accounts for between 3,000 and 33,000 lung cancer deaths in the United States each year, with central estimates of 15,400 or 21,800 (depending on the model used). This makes radon the second-leading cause of lung cancer after cigarette smoking, although cigarettes account for far more cases than radon.

Most radon-induced cases of lung cancer occur in smokers, reflecting synergy between smoking and radon exposure. Quitting smoking is an essential part of prevention, but the estimates of radon-caused lung cancer are also substantial.

Radon-induced lung cancer can be prevented by reducing radon levels in homes and other buildings. Approximately one-third of radon-induced lung cancer could be avoided if homes with radon concentrations exceeding 4 pCi/L (the EPA action level) underwent changes to reduce radon concentrations to below that level. However, eliminating all radon exposure is not possible.

Additional Resources

National Organizations and Web Sites

In addition to the American Cancer Society, other sources of patient information and support include*:

Environmental Protection Agency (EPA)
Internet Address: http://www.epa.gov/iaq/radon/
Useful EPA publications:
Radon: A Physician’s Guide (http://www.epa.gov/iaq/radon/pubs/physic.html)
A Citizen’s Guide to Radon: The Guide to Protecting Yourself and Your Family from Radon (http://www.epa.gov/iaq/radon/pubs/citguide.html)

Federal Radiation Exposure Compensation Program
Information available at: http://www.usdoj.gov/civil (click "Radiation Exposure Compensation Program" from the menu)

United States Geological Survey
Internet Address: http://www.usgs.gov/
General background on radon ("Radon in Earth, Air, and Water") and
maps of radon exposure potential available at:
http://energy.cr.usgs.gov/radon/radonhome.html

*Inclusion on this list does not imply endorsement by the American Cancer Society

Other Publications*

Axelson O. Cancer risk from exposure to radon in homes. Environ Health Perspect. 1995;103 :37-43.

Boice JD, Lubin JH. Occupational and environmental radiation and cancer. Cancer Causes Control 1997;8:309-322.

Lubin JH, Boice JD Jr, Edling C, et al. Lung cancer in radon-exposed miners and estimation of risk from indoor exposure. J Natl Cancer Inst. 1995;87:817-827.

Samet J. Radon and lung cancer. J Natl Cancer Inst. 1989;81:745-757.

Diesel Exhaust

Exposure to diesel exhaust is widespread in the modern world. Trucks, buses, trains, construction and farm equipment, generators, ships, and some cars have diesel engines. Exhaust from these engines brings a complex mixture of soot and gases to roadways, cities, farms, and other workplaces. Health concerns about diesel exhaust relate not only to cancer, but also to lung (respiratory) and heart diseases.

What Is Diesel Exhaust?

The exhaust from diesel engines is made up of both gases and soot, each of which is made up of thousands of different substances. The gas portion of diesel exhaust is mostly carbon dioxide, carbon monoxide, nitric oxide, nitrogen dioxide, sulfur oxides, and hydrocarbons, including polycyclic aromatic hydrocarbons (PAHs). The particulate portion of diesel exhaust, also known as soot, is mainly made up of elemental carbon, organic material (including PAHs), and traces of metallic compounds. So, PAHs are found in both the gases and the soot of diesel exhaust.

How Are People Exposed to Diesel Exhaust?

People are exposed to diesel exhaust by breathing in the soot and gases, rather than by eating contaminated foods or through skin absorption. Measuring exposure is difficult because diesel exhaust is chemically complex and many parts of it are also found in a lot of other sources. This has been, and remains, a major challenge in scientific studies. People may be exposed to diesel exhaust at work, through daily living, or on the way to school.

At Work

The amount and length of time people are exposed to diesel exhaust varies greatly. Those with the highest exposures include truck drivers, bridge and tunnel workers, mine workers, forklift drivers, railroad and dock workers, and garage workers. Farm workers and car, truck, and bus maintenance garage workers may also spend a lot of time around diesel exhaust.

Every Day

The general public is also exposed to diesel exhaust, although less often and at much lower levels than in the workplace. Exposures are highest where diesel traffic is heaviest, such as along major highways and in cities.

On the Way to School

One particular area of concern that has been studied is children’s exposures to diesel exhaust and other vehicle pollutants while going to school on diesel school buses. The California Environmental Protection Agency published the results of The Children’s School Bus Exposure Study in 2003. The study found that diesel exhaust exposure is indeed increased during bus travel and needs to be reduced. Many schools now use the study's suggestions of minimizing travel times; using the newest, cleanest buses for the longest trips; retiring older buses as quickly as possible; and decreasing bus-to-bus lineups and idling time in an effort to reduce children's exposure to bus-related air pollutants.

Does Diesel Exhaust Cause Cancer?

Background Information

How Normal Cells Become Cancer Cells

Cancer cells develop because of damage to DNA. DNA is in every cell and directs all the cell's activities. When DNA becomes damaged it is often able to repair itself. In cancer cells, the damage is not repaired.

Carcinogens

A substance that causes cancer is called a carcinogen (car-SIN-oh-gin). Some carcinogens do not act on DNA directly, but lead to cancer in other ways. For example, the carcinogen may cause cells to divide at a faster rate, which could increase the chances that DNA changes will occur.

Carcinogens do not cause cancer in every case, all the time. Substances classified as carcinogens may have different levels of cancer-causing potential. Some may cause cancer only after prolonged, high levels of exposure. And for any one person, the risk of developing cancer depends on many factors, such as the length and intensity of exposure to the carcinogen, the person's overall health, and the person’s family history.

Evidence

Two kinds of evidence tell us about the cancer-causing (carcinogenic) potential of diesel exhaust:

1. studies of the parts of diesel exhaust, such as soot and PAHs
2. studies of diesel exhaust itself

A full discussion of what is known about the parts of diesel exhaust, such as soot and PAHs, is beyond the scope of this article, but soot and PAHs have been classified as carcinogens. Evidence about diesel exhaust as a whole is presented here.

What Do Epidemiologic Studies Suggest?

Epidemiologic studies provide information about the possible causes of disease, occurrence of disease in a population or its subgroups, and trends in the frequency of disease over time. Epidemiologic studies of lung cancer risk in diesel-exposed workers have been done. Lung cancer is the major cancer thought to be linked to diesel exhaust.

These studies face the usual challenges of such studies. For example, it is very hard to correctly define and measure work-place exposure. It is also difficult to take into account the impact of other risk factors, such as smoking.

Epidemiologic studies of workers exposed to diesel exhaust have shown small but significant increases in risk of lung cancer. A case-control study found that railroad workers with at least 20 years of service were more likely to die from lung cancer than were members of the general population. Another study of railroad workers by the same researchers found that lung cancer risk increased with length of exposure to diesel exhaust; the relative risk was highest among workers with the longest exposure.

Several studies of Teamsters also linked diesel exhaust exposure with lung cancer. Still another study of almost a half-million American men looked at the effect of work-place exposure to diesel exhaust on their risk of developing lung cancer. Men with the heaviest and most prolonged exposures, such as railroad workers, heavy equipment operators, miners, and truck drivers, had higher lung cancer death rates than unexposed workers. Although most studies have found a link between diesel exhaust exposure and lung cancer, many have not. Still, with more than 1 million exposed workers, diesel exhaust may pose a substantial health risk.

The relationship between lung cancer and diesel exhaust in the general environment has been studied less than occupational exposures.

What Do Animal and Laboratory Studies Suggest?

In laboratory studies, diesel exhaust (as soot or chemical extracts) can cause changes in DNA. Several studies also provide proof that diesel exhaust can cause cancer in animals. For example, a long-term inhalation study in mice, rats, and hamsters exposed to diesel exhaust showed a higher rate of lung cancer in the exposed animals. However, the carcinogenic effects of diesel exhaust in animals may relate to soot overload in their lungs. If true, this would suggest that normal lung defenses must be overcome in order for diesel exhaust to cause cancer.

What Do the Experts Say?

Based on animal and human evidence, expert agencies have evaluated the potential of diesel exhaust to cause cancer.

The National Toxicology Program

The National Toxicology Program evaluates exposures that may cause cancer. Exposures that are thought to cause cancer are included in the "Reports on Carcinogens," which is published every 2 years. Each exposure is assigned to 1 of 2 categories: "known to be human carcinogens," and "reasonably anticipated to be human carcinogens." The first category includes substances for which human studies (epidemiologic and/or experimental studies) provide "sufficient evidence" that they cause cancer in humans. The second category includes substances for which there is limited evidence that they cause cancer in humans and/or sufficient evidence of causing cancer in experimental animals. In 2005, the National Toxicology Program classified diesel exhaust particulates as "reasonably anticipated to be human carcinogens."

The International Agency for Research on Cancer

The International Agency for Research on Cancer (IARC) also evaluates exposures that may cause cancer. IARC classifies exposures into 1 of 4 categories.

* Group-1 exposures are those "known to be carcinogenic to humans," usually based on "sufficient" human evidence, but sometimes based on "sufficient" evidence in experimental animals and "strong" human evidence.
* Group-2 exposures are divided into 2 categories. Group-2A ("probably carcinogenic to humans") has stronger evidence, and Group-2B ("possibly carcinogenic to humans") has weaker evidence.
* Group-3 exposures are not considered classifiable because the available evidence is limited or inadequate.
* Group-4 exposures are "probably not carcinogenic to humans" based on evidence suggesting these substances do not cause cancer in humans or in experimental animals.

IARC puts diesel exhaust in Group-2A, as "probably carcinogenic to humans."

The Environmental Protection Agency

The Environmental Protection Agency (EPA) uses a classification system very similar to that of the IARC. EPA considers diesel exhaust "likely to be carcinogenic to humans." The EPA also reports that the fine particles that diesel exhaust contains "are a serious risk to public health. They pose a significant health risk because they can pass through the nose and throat and become lodged in the lungs. Fine particles cause lung damage and premature death. They can also aggravate respiratory conditions such as asthma and bronchitis."

The National Institute for Occupational Safety and Health

Yet another expert agency, the National Institute for Occupational Safety and Health (NIOSH) "has determined that diesel exhaust is a potential human carcinogen, based on a combination of chemical, genotoxicity, and carcinogenicity data. In addition, acute exposures to diesel exhaust have been linked to health problems such as eye and nose irritation, headaches, nausea, and asthma." They go on to state that though the cancer-causing potential of diesel exhaust has not been measured, exposure should be minimized to reduce any possible cancer risk.

Does Diesel Exhaust Cause Any Other Health Problems?

Lung cancer is the main cancer to have been linked to diesel exhaust, but there is also suspicion that other cancers, especially those of the larynx, pancreas, bladder, and kidney, may be associated with diesel exhaust.

Diesel exhaust is a major part of outdoor air pollution. As mentioned above, diesel exhaust is believed to play a role in other health problems, such as eye irritation, headache, lung damage, asthma and other lung diseases, heart diseases, and possibly immune system problems.

What Should I Do If I Have Been Exposed to Diesel Exhaust?

If you are or have been heavily exposed to diesel fumes, your risk of lung cancer may be increased. If you have been exposed to diesel fumes in the general environment, the increase in your risk is likely to be very small. If you have had exposure to high levels over a long period of time, your risk is higher. However, using study results to predict individual problems is not easy, so measuring the exact amount of an exposed person’s risk is difficult.

At Work

If your workplace exposes you to diesel exhaust, there are many ways to reduce or prevent exposures. Some of these measures will also protect you from other chemical exposures that are likely to happen in the workplace. Engineering changes, such as ventilating the exhaust away from workers’ breathing zones, are important. Good work practices, such as changing clothes after work, washing hands regularly, and keeping food out of the work area, are also important. Finally, personal protective equipment, such as respirators, may be a key part of a workplace protective program. You should work with your employer to be sure that enough protection is in place.

For more information on preventing or reducing occupational exposures in your current job, consult your company’s safety and health manager. Additional technical assistance is available from the National Institute for Occupational Safety and Health (NIOSH).

Every Day

If you are exposed to diesel exhaust fumes in the general environment, you can take some of the same precautions. For example, you can avoid spending time near large sources of diesel exhaust, such as behind trucks and buses. Over the last 7 years the EPA has enforced the Clean Air Act, which included reducing diesel emissions from cars and trucks by mandated changes in both engines and fuel. This has decreased public exposure to diesel exhaust.

Cigarette smoking is a much more powerful risk factor for lung cancer than are diesel fumes. The two exposures combined, however, may increase risk to a greater extent than the sum of their individual risks. People with a history of diesel exhaust exposure should avoid any contact with tobacco smoke, either through smoking or through secondhand exposure.

What's the Bottom Line?

Prolonged exposure to diesel exhaust probably increases the risk of lung cancer and maybe other cancers, too. Parts of diesel exhaust, such as soot and PAHs, have been shown to cause cancer. As a result, several government and research organizations have stated that diesel exhaust probably causes cancer in humans. Another reason for limiting exposure is that diesel exhaust, like many other air pollutants, also causes lung, heart, and other health problems.

Short-term exposure to diesel exhaust is very unlikely to affect anyone's risk of developing lung cancer. However, US regulatory agencies, such as the EPA and OSHA, continue to look for ways to limit diesel exhaust exposures of the general public and of workers, because this exposure is common and the combined risk for the population overall may be considerable.

Secondhand Smoke

What Is Secondhand Smoke?

Secondhand smoke, also known as environmental tobacco smoke (ETS) or passive smoke, is a mixture of 2 forms of smoke from burning tobacco products:

* Sidestream smoke: smoke that comes from the end of a lighted cigarette, pipe, or cigar
* Mainstream smoke: smoke that is exhaled by a smoker

When non-smokers are exposed to secondhand smoke it is called involuntary smoking or passive smoking. Non-smokers exposed to secondhand smoke absorb nicotine and other toxic chemicals just like smokers do. The more secondhand smoke you are exposed to, the higher the level of these harmful chemicals in your body.

Why Is Secondhand Smoke a Problem?

Secondhand smoke is classified as a "known human carcinogen" (cancer-causing agent) by the US Environmental Protection Agency (EPA), the US National Toxicology Program, and the International Agency for Research on Cancer (IARC), a branch of the World Health Organization.

Tobacco smoke contains over 4,000 chemical compounds. More than 60 of these are known or suspected to cause cancer.

Secondhand smoke can be harmful in many ways. In the United States alone, each year it is responsible for:

* an estimated 35,000 deaths from heart disease in non-smokers who live with smokers
* about 3,400 lung cancer deaths in non-smoking adults
* other breathing problems in non-smokers, including coughing, mucus, chest discomfort, and reduced lung function
* 150,000 to 300,000 lung infections (such as pneumonia and bronchitis) in children younger than 18 months of age, which result in 7,500 to 15,000 hospitalizations
* increases in the number and severity of asthma attacks in about 200,000 to 1 million children who have asthma
* more than 750,000 middle ear infections in children

Pregnant women exposed to secondhand smoke are also at increased risk of having low birth weight babies.

An issue that continues to be studied is whether secondhand smoke may increase the risk of breast cancer. Both mainstream and secondhand smoke contain about 20 chemicals that, in high concentrations, cause breast cancer in rodents. Chemicals in tobacco smoke reach breast tissue and are found in breast milk.

The evidence regarding secondhand smoke and breast cancer risk in human studies is still being debated, partly because the risk has not been shown to be increased in active smokers. One possible explanation for this is that tobacco smoke may have different effects on breast cancer risk in smokers and in those who are exposed to secondhand smoke.

A report from the California Environmental Protection Agency in 2005 concluded that the evidence regarding secondhand smoke and breast cancer is "consistent with a causal association" in younger, mainly premenopausal women. The 2006 US Surgeon General's report, The Health Consequences of Involuntary Exposure to Tobacco Smoke, concluded that there is "suggestive but not sufficient" evidence of a link at this point. In any case, women should be told that this possible link to breast cancer is yet another reason to avoid contact with secondhand smoke.

The 2006 US Surgeon General's report reached several important conclusions:

* Secondhand smoke causes premature death and disease in children and in adults who do not smoke.
* Children exposed to secondhand smoke are at an increased risk of sudden infant death syndrome (SIDS), acute respiratory infections, ear problems, and more severe asthma. Smoking by parents causes breathing (respiratory) symptoms and slows lung growth in their children.
* Secondhand smoke immediately affects the heart and blood circulation in a harmful way. It also causes heart disease and lung cancer.
* The scientific evidence shows that there is no "safe" level of exposure to secondhand smoke.
* Many millions of Americans, both children and adults, are still exposed to secondhand smoke in their homes and workplaces despite a great deal of progress in tobacco control.
* The only way to fully protect non-smokers from exposure to secondhand smoke indoors is to prevent all smoking in that indoor space or building. Separating smokers from non-smokers, cleaning the air, and ventilating buildings cannot keep non-smokers from being exposed to secondhand smoke.

Where Is Secondhand Smoke a Problem?

There are 3 locations where you should be especially concerned about exposure to secondhand smoke:

Your Workplace

The workplace is a major source of secondhand smoke exposure for adults. Secondhand smoke meets the criteria to be classified as a potential cancer-causing agent by the Occupational Safety and Health Administration (OSHA), the federal agency responsible for health and safety regulations in the workplace. The National Institute for Occupational Safety and Health (NIOSH), another federal agency, also recommends that secondhand smoke be considered a potential occupational carcinogen. Because there are no known safe levels, they recommend that exposures to secondhand smoke be reduced to the lowest possible levels.

Secondhand smoke exposure in the workplace has been linked to an increased risk for heart disease and lung cancer among adult non-smokers. The Surgeon General has concluded that smoke-free workplace policies are the only effective way to do away with secondhand smoke exposure in the workplace. Separating smokers from non-smokers, cleaning the air, and ventilating the building cannot prevent exposure if people smoke inside the building. Aside from protecting non-smokers, workplace smoking restrictions may also encourage smokers who wish to quit or reduce their use of tobacco products.

Public Places

Everyone can be exposed to secondhand smoke in public places, such as restaurants, shopping centers, public transportation, schools, and daycare centers. Although some businesses are reluctant to ban smoking, there is no credible evidence that going smoke-free is bad for business. Public places where children go are a special area of concern.

Your Home

Making your home smoke-free may be one of the most important things you can do for the health of your family. Any family member can develop health problems related to secondhand smoke. Children are especially sensitive. In the United States, 21 million, or 35% of children live in homes where residents or visitors smoke in the home on a regular basis. About 50% to 75% of children in the United States have detectable levels of cotinine, the breakdown product of nicotine, in their blood.

Think about it: we spend more time at home than anywhere else. A smoke-free home protects your family, your guests, and even your pets.

What About Smoking Odors?

There is no research in the medical literature about the cancer-causing effects of cigarette odors. The literature does show that secondhand tobacco smoke can get into hair, clothing, and other surfaces. Though unknown, the cancer-causing effects would likely be very small compared to direct exposure to secondhand smoke, such as living in a house with a smoker.

What Can Be Done About Secondhand Smoke?

Local, state, and federal authorities can enact public policies to protect people from secondhand smoke and protect children from tobacco-caused diseases and addiction. Because there are no safe levels of secondhand smoke, it is important that any such policies be as strong as possible, and that they do not prevent action at other levels of government.

Many US local and state governments, and even federal governments in some other countries, have decided that protecting the health of employees and others in public places is of the utmost importance. And many have passed clean indoor air laws in recent years. While the laws vary from place to place, they are becoming more common. Detailed information on smoking restrictions in each state is available from the American Lung Association at http://slati.lungusa.org.

To learn how you can become involved in reducing exposure to secondhand smoke, contact your American Cancer Society at 1-800-ACS-2345 (1-800-227-2345).

Cigarette Smoking

Introduction


The 1982 United States Surgeon General's Report stated that "Cigarette smoking is the major single cause of cancer mortality in the United States." This statement is as true today as it was in 1982.


Smoking is responsible for nearly 1 in 5 deaths in the United States. Because cigarette smoking and tobacco use are acquired behaviors -- activities that people choose to do -- smoking is the most preventable cause of premature death in our society.


This document gives a brief overview of cigarette smoking: who smokes, how smoking affects health, what makes it so hard to quit, and what some of the many benefits of quitting are. For more information on this topic, see the American Cancer Society document, Guide to Quitting Smoking.


Who Smokes?

According to the Centers for Disease Control and Prevention (CDC), 44.5 million US adults were current smokers in 2006 (the most recent year for which numbers are available). This is 20.8% of all adults (23.9% of men, 18.0% of women) -- more than 1 out of 5 people.

When broken down by race/ethnicity, the numbers were as follows:

Whites 21.9%
African Americans 23.0%
Hispanics 15.2%
American Indians/Alaska Natives 32.4%
Asian Americans 10.4%

The numbers were higher in younger age groups. In 2006, CDC reported almost 24% of those 18 to 44 years old were current smokers, compared to 10.2% in those aged 65 or older.

Nationwide, 22.3% of high school students and 8.1% of middle school students were smoking in 2004. More White and Hispanic students smoked cigarettes. (For more information, see the American Cancer Society document, Child and Teen Tobacco Use.)

Health Effects of Smoking

About half of all Americans who continue to smoke will die because of the habit. Each year about 440,000 people in the United States die from illnesses related to cigarette smoking. Cigarettes kill more Americans than alcohol, car accidents, suicide, AIDS, homicide, and illegal drugs combined.

Cancer

Cigarette smoking accounts for at least 30% of all cancer deaths. It is a major cause of cancers of the lung, larynx (voice box), oral cavity, pharynx (throat), esophagus (swallowing tube connected to the stomach), and bladder, and it contributes to the development of cancers of the pancreas, cervix, kidney, stomach, and also some leukemias.

Smoking is responsible for about 87% of lung cancer deaths. Lung cancer is the leading cause of cancer death in both men and women, and is one of the most difficult cancers to treat. Lung cancer is a disease that can in many cases be prevented. Groups that promote non-smoking as part of their religion, such as Mormons and Seventh-day Adventists, have much lower rates of lung cancer and other smoking-related cancers.

Other Health Problems

Only about half of the deaths related to smoking are from cancer. Smoking is also a major cause of heart disease, aneurysms, bronchitis, emphysema, and stroke, and it makes pneumonia and asthma worse.

Using tobacco can also damage a woman's reproductive health. Tobacco use is linked with reduced fertility and a higher risk of miscarriage, early delivery (premature birth), stillbirth, infant death, and is a cause of low birth-weight in infants. It has also been linked to sudden infant death syndrome (SIDS).

Smoking has also been linked to other health problems, including gum disease, cataracts, bone thinning, hip fractures, and peptic ulcers. It is also linked to macular degeneration, an eye disease that can cause blindness.

Furthermore, the smoke from cigarettes (called secondhand smoke or environmental tobacco smoke) has a harmful health effect on those exposed to it. (See the American Cancer Society documents, Secondhand Smoke and Women and Smoking.)

Effects on Quantity and Quality of Life

Based on data collected from 1995 to 1999, the CDC estimated that adult male smokers lost an average of 13.2 years of life and female smokers lost 14.5 years of life because of smoking.

But not all of the health problems related to smoking result in deaths. Smoking generally affects a smoker's health, harming nearly every organ of the body, and causing many diseases. According to the CDC in 2000, about 8.6 million people had at least one chronic disease because they smoked or had smoked. Many of these people were suffering from more than one smoking-related condition. The diseases that occurred most often were chronic bronchitis, emphysema, heart attacks, strokes, and cancer. These diseases can steal away a person's quality of life long before death. Smoking-related illness can limit a person's activities by making it harder to breathe, get around, work, or play.

Taking Care of Yourself

If you have used tobacco in any form, now or in the past, tell your health care provider so he or she can be sure that you have right preventive health care. It is well known that smoking puts you at risk for certain health-related illnesses. This means part of your health care should focus on related screening and preventive measures to help you stay as healthy as possible. For example, you will want to regularly check the inside of your mouth for any changes and have an oral exam by your doctor or dentist if you do find any changes or problems. The American Cancer Society recommends that periodic check-ups should include oral cavity (mouth) exams. By doing this tobacco users may be able to find oral changes and leukoplakia (white patches on the mouth membranes) early. This may help prevent oral cancer.

You should also be aware of any of the following:

* any change in a cough (for example, you cough up more phlegm than usual)
* a new cough
* coughing up blood
* hoarseness
* trouble breathing
* wheezing
* headaches
* chest pain
* loss of appetite
* weight loss
* general fatigue (feeling tired all the time)
* repeated respiratory infections

Any of these could be signs of lung cancer or a number of other lung conditions and you should report any symptom to your doctor. Although these can be signs of a problem, many lung cancers do not cause any noticeable symptoms until they are advanced and have spread to other parts of the body.

If you have any health concerns that you think may be related to your cigarette smoking, please see your health care provider as quickly as possible. Taking care of yourself and getting treatment for small problems will give you the best chance for successful treatment. The best way, though, to take care of yourself and decrease your risk for life-threatening lung problems is to quit smoking.

Ingredients in Tobacco

Cigarettes, cigars, and spit and pipe tobacco are made from dried tobacco leaves, as well as ingredients added for flavor and other properties. More than 4,000 individual chemicals have been identified in tobacco and tobacco smoke. Among these are more than 60 chemicals that are known carcinogens (cancer-causing agents).

There are hundreds of substances added to cigarettes by manufacturers to enhance the flavor or to make the smoking experience more pleasant. Some of the compounds found in tobacco smoke include ammonia, tar, and carbon monoxide. Exactly what effects these substances have on the cigarette smoker’s health is unknown, but there is no evidence that lowering the tar content of a cigarette improves the health risk. Manufacturers do not usually give out information to the public about the additives used in cigarettes, so it is hard to know the health risks.

Nicotine Addiction

Addiction is characterized by the repeated, compulsive seeking or use of a substance despite its harmful effects and consequences. Addiction is defined as physical and psychological dependence on the substance. Nicotine is the addictive drug in tobacco. Regular use of tobacco products leads to addiction in a high proportion of users.

In 1988, the US Surgeon General concluded the following:

* Cigarettes and other forms of tobacco are addicting.
* Nicotine is the addicting drug in tobacco.
* The ways people become addicted to tobacco are similar to those that for addiction to other drugs such as heroin and cocaine.

Nicotine is found in substantial amounts in all forms of tobacco. It is absorbed readily through the lungs with cigarette smoking and through the mouth or nose with oral tobacco. From these entry points, nicotine quickly spreads throughout the body.

Tobacco companies are required by law to report nicotine levels in cigarettes to the Federal Trade Commission (FTC), but in most states they are not required to show the amount of nicotine on the cigarette package label. The actual amount of nicotine available to the smoker in a given brand of cigarettes is often different from the level reported to the FTC. In one regular cigarette, the average amount of nicotine the smoker gets ranges between about 1 mg and 2 mg.

Although 70% of smokers want to quit and more than 40% try to quit each year, fewer than 5% succeed. This is because smokers not only become physically addicted to nicotine; there is a strong emotional (psychological) aspect and they often link smoking with many social activities. All of these factors make smoking a hard habit to break.

Benefits of Quitting Smoking

Nicotine is a very addictive drug. People usually try to quit many times before they are successful. In September 1990, the US Surgeon General outlined the benefits of quitting smoking:

* Quitting smoking has major and immediate health benefits for people with and without smoking-related disease.
* Former smokers live longer than continuing smokers. For example, people who quit smoking before age 50 have one-half the risk of dying in the next 15 years compared with people who keep smoking.
* Quitting smoking decreases the risk of lung cancer, other cancers, heart attack, stroke, and chronic lung diseases such as emphysema and chronic bronchitis.
* Women who stop smoking before pregnancy or during the first 3 to 4 months of pregnancy reduce their risk of having a low birth-weight baby to that of women who never smoked.
* The health benefits of quitting smoking are far greater than any risks from the small weight gain (usually less than 10 pounds) or any emotional or psychological problems that may follow quitting.

Your risk of having lung cancer and other smoking-related cancers is affected by how much you have been exposed to cigarette smoke over your lifetime. This is measured by the number of cigarettes you smoked each day, how old you were when you started smoking, and the number of years you have smoked. There is no way to accurately calculate a person's risk of getting cancer, but the more you smoke and the longer you do it, the greater your risk.

The good news is that the risk of having lung cancer and other smoking-related illnesses can be reduced if you stop smoking. The risk of lung cancer is less in people who quit smoking than in people who continue to smoke the same number of cigarettes every day, and the risk decreases as the number of years since quitting increases.

People who stop smoking when they are young get the greatest health benefits from quitting. Those who quit in their 30s may avoid most of the risk due to tobacco use. However, even smokers who quit after age 50 largely reduce their risk of dying early. The argument that it is too late to quit smoking because the damage is already done is not true. It is never too late to quit smoking!

For more information, see the American Cancer Society document, Guide to Quitting Smoking.

Additional Resources

More Information from Your American Cancer Society

The following information may also be helpful to you. These materials may be ordered from our toll-free number, 1-800-ACS-2345 (1-800-227-2345).

Child and Teen Tobacco Use (also available in Spanish)

Cigar Smoking (also available in Spanish)

Guide to Quitting Smoking (also available in Spanish)

Double Your Chances of Quitting Smoking

Helping a Smoker Quit: Dos and Don'ts

Questions About Smoking, Tobacco, and Health (also available in Spanish)

Quitting Smoking - Help for Cravings and Tough Situations (also available in Spanish)

Secondhand Smoke (also available in Spanish)

Women and Smoking (also available in Spanish)

National Organizations and Web Sites

In addition to the American Cancer Society, other sources of information and support include:

American Heart Association & American Stroke Association
Heart Association: 1-800-AHA-USA-1 (1-800-242-8721)
Internet Address: www.americanheart.org
Stroke Association: 1-888-4-STROKE (1-888-478-7653)
Internet Address: www.strokeassociation.org

American Lung Association
1-800-LUNG-USA (1-800-586-4872)
Internet Address: www.lungusa.org

Centers for Disease Control and Prevention (CDC)
Office of Smoking And Health
Telephone: 1-800-232-4636 (1-800-CDC-INFO)
Internet Address: www.cdc.gov/tobacco/quit_smoking/index.htm

National Cancer Institute
1-800-4-CANCER (1-800-422-6237) – Answers as "Cancer Information Service"
Internet Address: www.cancer.gov

Nicotine Anonymous
1-877-TRY-NICA (1-877-879-6422)
Internet Address: www.nicotine-anonymous.org

Smokefree.gov
(Info on state Quitlines)
Telephone: 1-800-QUITNOW (1-800-784-8669)
Internet Address: www.smokefree.gov

*Inclusion on this list does not imply endorsement by the American Cancer Society.

The American Cancer Society is happy to address almost any cancer-related topic. If you have any more questions, please call us at 1-800-ACS-2345 any time, 24 hours a day.

Tobacco Ingredient and Nicotine Reporting

Description of the Laws: The Federal Cigarette Labeling and Advertising Act (FCLAA) and Comprehensive Smokeless Tobacco Health Education Act (CSTHEA)


Cigarettes


The Federal Cigarette Labeling and Advertising Act (FCLAA), 15 U.S.C. §1335a(a), Public Law 89–92, in part requires that each person who manufactures, packages, or imports cigarettes annually submit to the Department of Health and Human Services (HHS) a list of ingredients added to tobacco in the manufacture of cigarettes (Ingredient Report). The Centers for Disease Control and Prevention (CDC), Office on Smoking and Health (OSH), has been delegated the responsibility of implementing these provisions. The Ingredient Report must include all additives and flavors. Submissions are due to CDC, OSH by March 31; and for importers, the Ingredient Report is also due upon initial importation into the United States. The report submitted by March 31st each year must represent the ingredients added to tobacco in the manufacture of cigarettes during the previous calendar year.

Under FCLAA, one may submit information which does not identify the company that uses the ingredients or the brand of cigarettes that contain the ingredients. A person or group of persons required to provide the ingredient list may designate an individual or entity to provide the list. In the event that another individual or entity, such as an attorney or counsel, is designated to submit this information on your behalf, this individual or entity should clearly state the name(s) of the importer(s) or company(ies) for whom they are submitting the information.


Smokeless Tobacco


The Comprehensive Smokeless Tobacco Health Education Act (CSTHEA), 15 U.S.C. §4403(a)(A), Public Law 99–252, in part requires each manufacturer, packager, or importer of smokeless tobacco products to annually submit to HHS the list of ingredients added to tobacco in the manufacture of smokeless tobacco products (Ingredient Report). CSTHEA, 15 U.S.C. §4403(a)(1)(B), further requires the submission of the quantity of nicotine contained in each smokeless tobacco product (Nicotine Report). CDC, OSH has been delegated the responsibility of implementing these provisions. Submissions are due to CDC, OSH by March 31; and for importers, the Ingredient Report is also due upon initial importation into the United States. The reports submitted by March 31st each year must represent the ingredients added to tobacco in the manufacture of smokeless tobacco during the previous calendar year; and the specification of the quantity of nicotine contained in smokeless tobacco products manufactured or imported during the previous calendar year.

Under CSTHEA, one may submit information which does not identify the company that uses the ingredients or the brand of smokeless tobacco that contains the ingredients. A person or group of persons required to provide the nicotine data and ingredient list may designate an individual or entity to provide the list. In the event that you designate another individual or entity, such as an attorney or counsel, to submit this information on your behalf, this individual or entity should clearly state the name(s) of the company(ies) for whom they are submitting the information.

понедельник, 22 октября 2007 г.

Youth and Cigarette Smoking

Introduction

This Factsheet covers only cigarette smoking among children and young people.

In 1996, Peto et al. estimated that unless current trends changed, some 30-40% of the 2.3 billion children and teenagers in the world would become smokers in early adult life . Unless action is taken now, about 250 million of these future smokers will be killed by smoking.

In countries where smoking is long established, almost all smokers begin before age 18 years. Young people are therefore an important focus for action. Trends in smoking among young people follow those in adults. Men take up smoking first, and boys follow them. Women are next, and girls follow them. In the USA, Canada, Australasia and Northern Europe, the epidemic is established, and smoking is found among all four groups.

In Africa, Asia, South America and certain areas of Southern Europe, the epidemic is at an earlier stage and smoking may be found predominantly among men. Here, social influences and the tobacco industry's promotional strategy must be seriously addressed immediately if the smoking epidemic is to be prevented.
The effects of smoking on young people

Addiction

Many young smokers think they can quit easily, but find that they are already addicted. Young smokers develop withdrawal symptoms when they stop smoking. Smokers as young as 12 years may already made unsuccessful attempts to quit. A survey in the UK found that two-thirds of smokers aged 16-19 years had unsuccessfully attempted to stop, most having tried several times.

Long-term health risks

Long-term health risks are increased when regular smoking begins during childhood or adolescence. For example, the earlier regular smoking starts, the greater the risk of lung cancer. The highest risk of lung cancer and of heart and circulatory diseases to in adulthood is seen in those who started to smoke regularly before age 15.

Immediate health effects

Many health problems develop very quickly in the young smoker: for example, respiratory diseases, heart and circulatory problems, and reduced immunity. Children who smoke are more often absent from school, as the result both of smoking-related ailments and for truancy and suspension. The likelihood of absence increases if their parents also smoke. Young smokers are also less fit than their non-smoking peers, because carbon monoxide from tobacco smoke replaces some of the oxygen in their blood.
Stages in youth smoking
Stages in youth smoking

Young smokers go through a series of stages. Each stage is influenced by different factors: any action developed to prevent youth smoking must address these influences. Note that this is not a one-way process: rather, the stages are fluid and may reverse and restart several times.

Precontemplation - the child is not thinking about smoking, but receives messages about it. At this stage, parental and siblings' smoking, advertising, films, television and role models all exert an influence.

Contemplation - received images or peer influence build up to a point where curiosity takes over and the young person considers trying a cigarette. Friends' behaviour is now added to the precontemplation influences.

Initiation - most young people try smoking, but the majority do not become regular smokers. At this stage, friends are usually the strongest influence.

Experimentation - involving repeated attempts to smoke. Young people may become addicted to nicotine after smoking a very small number of cheap cigarettes, which may be why many experimenters become regular smokers. At this stage, peer-bonding is still the strongest influence.

Regular smoking - may involve a new set of influences. As well as addiction and habituation, personal factors such as beliefs about the benefits of smoking, self-efficacy, self-perception and coping join earlier influences. Societal factors including price and availability, and interpersonal factors such as school policy, provide a background.

Maintenance - continuation of regular smoking involves all these influences, but addiction is a major force.

Quitting - occurs when the relative importance of influences changes. For example, a new non-smoking partner, steep increases in the price of cigarettes, decreases in spending money, and beginning work where smoking is not permitted can all trigger a decision to stop.
Why do young people smoke and what can be done to prevent it?

The onset and maintenance of smoking is clearly complex. Here, we discuss selected findings from research in industrialised countries. As these may not apply elsewhere, each country should carry out research to identify areas in which effective action can be developed.

Suggestion for action

Carry out regular surveys with representative samples of young people as a baseline for planning e.g. every two years. WHO can advise on this.

Conducting a smoking prevalence survey

Introduction

How much tobacco people use and the way in which they use it-whether they smoke manufactured cigarettes, chew snuff or spit tobacco, smoke pipes, or roll their own cigarettes-varies widely both across countries and between groups within a country. There is tremendous variation even in patterns and levels of the smoking of manufactured cigarettes, the most common form of tobacco use.

Numerous studies have shown that these differences reflect the influence of environmental factors. The tobacco industry conducts very effective promotional campaigns to encourage adolescents, in particular, to smoke. Once addicted, smokers find it difficult to quit - continual reinforcement of health information and messages, as well as incentives, are needed to help smokers persevere with quitting until their attempts to stop are successful.

Differences in smoking patterns translate eventually into differences in population morbidity and mortality. Several studies have calculated the resultant social costs of smoking. In the United States of America, such studies have been used to justify increases in cigarette excise taxes, which often support state-level tobacco control programs. Increases in cigarette prices through excise taxes also result in reductions in smoking prevalence. Thus, just as public policy can influence smoking behaviour, the prevalence of smoking can also have a profound impact on public policy and finance.

Whether designing, monitoring or advocating tobacco control programmes, the availability of reliable data on smoking prevalence is crucial.
What is a smoking prevalence survey?

The main aim of a smoking prevalence survey is to characterize the current smoking behaviour of a given population, and of sub-populations of interest. Such surveys may also monitor exposure to variables that are known to influence smoking, such as the price of tobacco, any restrictions on smoking, and receptivity to tobacco industry messages.
How representative of the population is the sample to be surveyed?

The key issue in all surveys of smoking prevalence is how well the survey represents the population. A representative study depends on surveying a sufficiently large and random sample of the total population of interest.

In communities where almost all households have a telephone, surveys carried out by dialling telephone numbers at random (random digit dialing) are reasonably sure to give each individual in the population an equal chance of being selected. Elsewhere, surveys are typically undertaken by an interviewer who visits a random sample of homes (again, the survey should be designed so that each home has an equal chance of being included). In both these types of surveys, smoking prevalence can be collected by a respondent reporting on all adults in the household, however, detailed smoking practices is usually valid only when collected from self-respondents.

When the population of interest is children or younger adolescents, school-based surveys can provide a practical means of obtaining a representative sample. The questionnaire is usually completed by the student themselves, although the survey questions may be read out to the entire class simulataneously. If information on adolescent smoking is collected directly from households, it will be necessary to include many more homes to obtain the desired final sample size, as not every household contains adolescents (in the United States of America, approximately six times as many households will need to be included).

While no survey is perfectly representative, slight deviations from non-random sampling can be compensated for by statistical methods that weight the results to adjust for under-represented groups. It is strongly recommended that expert statistical advice be obtained during the initial design stages of the survey, as well as during the analysis of the data collected.
How large a sample is needed?

The size of the sample required will depend on the level of precision required in the results - a larger sample size will allow a more accurate estimate of the true prevalence of smoking in the population being sampled. The final decision on sample size should be made on the basis of the results of an analysis of the statistical power of the key research questions. This should be undertaken by a statistical expert.
What questions should the survey include?

Smoking prevalence

Smoking prevalence is usually reported separately for adults and for adolescents. A prevalence measure gives a picture of smoking among the population at a given time, and is often likened to a photographic snapshot.

In reality, however, tobacco use is dynamic. It takes time to become addicted to tobacco, and much, much longer to break the addiction. Moreover, the health consequences of smoking vary with length of exposure and persist to varying degrees even after tobacco use ceases. For these reasons, it is important to obtain data on previous as well as current tobacco use. In addition, to evaluate the effectiveness of interventions, it is important to ask questions that will detect changes in patterns of initiation and quitting. A critical point often ignored in prevalence surveys is to ensure that exactly the same the questions are asked in sucessive surveys so that inferences on changes in population behaviour can be drawn.

Prevalence and patterns of use among specific populations may be of particular interest. For example, patterns of tobacco use among physicians may indicate the likelihood of future change among the general population. are important health role models. Where is high, patients are both less likely to be advised to stop smoking, and less likely to accept that smoking is . The trends in smoking among medical students may also be an important indicator, as it The Tobacco Control Resource Centre is coordinating an international prevalence survey of smoking among physicians across Europe, and has developed and tested a standardised methodology for prevalence surveys anmong doctors. Visit the TCRC internet site for more details (htpp://www.tobacco-control.org/).

Other important groups include minority or ethnic groups who may not be reached equally by health promotion messages. Differences in prevalence in specific population subgroups can be used to demonstrate the need for focussed interventions.

All smoking surveys should gather sociodemographic information. At a minimum, this should include data on age, gender, educational level and socioeconomic status. Different trends in smoking by educational level, for example, can indicate the rate of diffusion of smoking initiation or cessation across the population. Before it was widely known that smoking was harmful, more priviledged social groups were the first to take up smoking. Since then, this group have led the population in giving up smoking. One aim for a tobacco control programme can be to minimize the difference in initation and cessation levels across social groups.
Smoking cessation

It is also important to monitor predictors of quitting. Smokers usually make several attempts to quit before they succeed. Among former smokers, the time of abstinence from cheap cigarettes is the most important indicator of the probability of relapse. Relapse is very high in the first few weeks after stopping smoking, but declines considerably thereafter. Ex-smokers who have abstained for a 12-month period have about a 5% risk of relapsing, so 12 months of continuous abstinence is often used as the criterion for successful quitting.

Tobacco control programs often aim to influence the behaviour of 'hard core' smokers, so it is useful to monitor their prevalence in the population. There are a number of ways of identifying such smokers. One approach is to determine how many smokers have never thought about quitting, have never tried to quit, and have no intention of doing so in the foreseeable future.

Among smokers who wish to quit, the level of nicotine addiction - as measured by number of cigarettes smoked each day and the time between waking and smoking the first cigarette - is an important predictor of the liklihood of a successful quit attempt. Past success in staying abstinent is also an important indicator. Availability of and willingness to use recommended medications during quitting is also associated with success. A thorough surveillance system will monitor each of these variables.