lung cancer essay introduction

Introduction to Lung Cancer

Lung cancer is the second most common cancer , accounting for about one out of five malignancies in men and one out of nine in women. Unfortunately, over the past several years, while the incidence of lung cancer has gradually declined in men, it has been rising alarmingly in women. In 1940 only seven women in 100,000 developed the disease; today the rate is 42 in 100,000. And all the evidence points to smoking as the cause. As one specialist in the field reports, "How long it takes to get cancer depends on how many cigarettes you smoke a day." However, studies prove that quitting smoking does lower the risk .

There are two major types of lung cancer: small cell lung cancer (SCLC)—which is also called oat cell cancer, because the cells resemble oat grains—and non-small cell lung cancer (NSCLC). The aggressiveness of the disease and treatment options depend on the type of tumor diagnosed. Because many types of lung cancer grow quickly and spread rapidly and because the lungs are vital organs, early detection and prompt treatment—usually surgery to remove the tumor—is critical.

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Health Encyclopedia

Lung cancer: introduction, what is cancer.

Cancer may seem complex. But at its core, cancer is simple. Normal cells grow and die when your body needs them to. Cancer is what happens when certain cells grow even though your body doesn’t need them.

In many cases, these cancerous cells form a lump or mass called a tumor. Since cancerous cells don’t act like normal cells, tumors can prevent your body from working correctly. Given time, they can also spread, or metastasize, to other parts of the body.

Lung cancer is cancer that starts in the cells that make up the lungs. It isn’t cancer that spreads to the lungs from other parts of the body. This is key because treatment is based on the original site of the tumor. For example: If a tumor begins in the breast and spreads to the lungs, it would be treated as metastatic breast cancer—not lung cancer.

Understanding the lungs

The lungs are sponge-like organs in your chest. Their job is to bring oxygen into the body and to get rid of carbon dioxide. When you breathe air in, it goes into your lungs through your windpipe (trachea). The trachea divides into tubes called bronchi, which enter the lungs. These divide into smaller branches called bronchioles. At the end of the bronchioles are tiny air sacs called alveoli. The alveoli move oxygen from the air into your blood. They take carbon dioxide out of the blood. This leaves your body when you breathe out (exhale).

Your right lung is divided into 3 sections (lobes). Your left lung has 2 lobes.

Types of lung cancer

There are two main types of lung cancer: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Understanding the differences between these types may lessen anxiety about your diagnosis and treatment.

Non-small cell lung cancer

NSCLC accounts for 85% to 90% of lung cancer cases. There are 3 main subtypes. Each subtype is named for the type of cell it develops in:

Adenocarcinoma. This is the most common type of lung cancer—particularly among the minority of non-smokers who get the disease. It tends to appear on the outer edges of the lungs and grows more slowly than the other subtypes. 

Squamous cell carcinoma (epidermoid carcinoma). This type of cancer develops more often in smokers or former smokers than lifetime nonsmokers. It tends to start in the center of the lungs near the bronchial tubes.

Large cell carcinoma.  The least common NSCLC, large cell carcinoma can begin anywhere in the lung. It tends to grow more quickly than the other subtypes, which can make it harder to treat.

Despite minor differences, they are often treated the same way.

Small cell lung cancer

Only about 1 in 10 to 3 in 20 people diagnosed with lung cancer have small-cell lung cancer (also called oat cell cancer). It's also almost exclusively found in smokers. It tends to grow more quickly than NSCLC. It often spreads to other parts of the body at an earlier stage.

How lung cancer spreads

Lung cancer acts differently in different people. But when it spreads, it tends to go to the same places. First: lymph nodes in the center of the chest. It may also spread to lymph nodes in the lower neck.

Lymph nodes are small clusters of immune system cells.

During later stages, lung cancer may spread to more distant parts of the body, such as the liver, brain, or bones.

Talk with your healthcare provider

If you have questions about lung cancer, talk with your healthcare provider. They can help you understand more about this cancer. 

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Lung cancer begins in the cells of your lungs.

Lung cancer is a type of cancer that begins in the lungs. Your lungs are two spongy organs in your chest that take in oxygen when you inhale and release carbon dioxide when you exhale.

Lung cancer is the leading cause of cancer deaths worldwide.

People who smoke have the greatest risk of lung cancer, though lung cancer can also occur in people who have never smoked. The risk of lung cancer increases with the length of time and number of cigarettes you've smoked. If you quit smoking, even after smoking for many years, you can significantly reduce your chances of developing lung cancer.

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Lung cancer typically doesn't cause signs and symptoms in its earliest stages. Signs and symptoms of lung cancer typically occur when the disease is advanced.

Signs and symptoms of lung cancer may include:

• A new cough that doesn't go away
• Coughing up blood, even a small amount
• Shortness of breath
• Losing weight without trying

When to see a doctor

Make an appointment with your doctor if you have any persistent signs or symptoms that worry you.

If you smoke and have been unable to quit, make an appointment with your doctor. Your doctor can recommend strategies for quitting smoking, such as counseling, medications and nicotine replacement products.

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Smoking causes the majority of lung cancers — both in smokers and in people exposed to secondhand smoke. But lung cancer also occurs in people who never smoked and in those who never had prolonged exposure to secondhand smoke. In these cases, there may be no clear cause of lung cancer.

How smoking causes lung cancer

Doctors believe smoking causes lung cancer by damaging the cells that line the lungs. When you inhale cigarette smoke, which is full of cancer-causing substances (carcinogens), changes in the lung tissue begin almost immediately.

At first your body may be able to repair this damage. But with each repeated exposure, normal cells that line your lungs are increasingly damaged. Over time, the damage causes cells to act abnormally and eventually cancer may develop.

Types of lung cancer

Doctors divide lung cancer into two major types based on the appearance of lung cancer cells under the microscope. Your doctor makes treatment decisions based on which major type of lung cancer you have.

The two general types of lung cancer include:

• Small cell lung cancer. Small cell lung cancer occurs almost exclusively in heavy smokers and is less common than non-small cell lung cancer.
• Non-small cell lung cancer. Non-small cell lung cancer is an umbrella term for several types of lung cancers. Non-small cell lung cancers include squamous cell carcinoma, adenocarcinoma and large cell carcinoma.

Risk factors

A number of factors may increase your risk of lung cancer. Some risk factors can be controlled, for instance, by quitting smoking. And other factors can't be controlled, such as your family history.

Risk factors for lung cancer include:

• Smoking. Your risk of lung cancer increases with the number of cigarettes you smoke each day and the number of years you have smoked. Quitting at any age can significantly lower your risk of developing lung cancer.
• Exposure to secondhand smoke. Even if you don't smoke, your risk of lung cancer increases if you're exposed to secondhand smoke.
• Previous radiation therapy. If you've undergone radiation therapy to the chest for another type of cancer, you may have an increased risk of developing lung cancer.
• Exposure to radon gas. Radon is produced by the natural breakdown of uranium in soil, rock and water that eventually becomes part of the air you breathe. Unsafe levels of radon can accumulate in any building, including homes.
• Exposure to asbestos and other carcinogens. Workplace exposure to asbestos and other substances known to cause cancer — such as arsenic, chromium and nickel — can increase your risk of developing lung cancer, especially if you're a smoker.
• Family history of lung cancer. People with a parent, sibling or child with lung cancer have an increased risk of the disease.

Complications

Lung cancer can cause complications, such as:

• Shortness of breath. People with lung cancer can experience shortness of breath if cancer grows to block the major airways. Lung cancer can also cause fluid to accumulate around the lungs, making it harder for the affected lung to expand fully when you inhale.
• Coughing up blood. Lung cancer can cause bleeding in the airway, which can cause you to cough up blood (hemoptysis). Sometimes bleeding can become severe. Treatments are available to control bleeding.
• Pain. Advanced lung cancer that spreads to the lining of a lung or to another area of the body, such as a bone, can cause pain. Tell your doctor if you experience pain, as many treatments are available to control pain.

Fluid in the chest (pleural effusion). Lung cancer can cause fluid to accumulate in the space that surrounds the affected lung in the chest cavity (pleural space).

Fluid accumulating in the chest can cause shortness of breath. Treatments are available to drain the fluid from your chest and reduce the risk that pleural effusion will occur again.

Cancer that spreads to other parts of the body (metastasis). Lung cancer often spreads (metastasizes) to other parts of the body, such as the brain and the bones.

Cancer that spreads can cause pain, nausea, headaches, or other signs and symptoms depending on what organ is affected. Once lung cancer has spread beyond the lungs, it's generally not curable. Treatments are available to decrease signs and symptoms and to help you live longer.

There's no sure way to prevent lung cancer, but you can reduce your risk if you:

• Don't smoke. If you've never smoked, don't start. Talk to your children about not smoking so that they can understand how to avoid this major risk factor for lung cancer. Begin conversations about the dangers of smoking with your children early so that they know how to react to peer pressure.
• Stop smoking. Stop smoking now. Quitting reduces your risk of lung cancer, even if you've smoked for years. Talk to your doctor about strategies and stop-smoking aids that can help you quit. Options include nicotine replacement products, medications and support groups.
• Avoid secondhand smoke. If you live or work with a smoker, urge him or her to quit. At the very least, ask him or her to smoke outside. Avoid areas where people smoke, such as bars and restaurants, and seek out smoke-free options.
• Test your home for radon. Have the radon levels in your home checked, especially if you live in an area where radon is known to be a problem. High radon levels can be remedied to make your home safer. For information on radon testing, contact your local department of public health or a local chapter of the American Lung Association.
• Avoid carcinogens at work. Take precautions to protect yourself from exposure to toxic chemicals at work. Follow your employer's precautions. For instance, if you're given a face mask for protection, always wear it. Ask your doctor what more you can do to protect yourself at work. Your risk of lung damage from workplace carcinogens increases if you smoke.
• Eat a diet full of fruits and vegetables. Choose a healthy diet with a variety of fruits and vegetables. Food sources of vitamins and nutrients are best. Avoid taking large doses of vitamins in pill form, as they may be harmful. For instance, researchers hoping to reduce the risk of lung cancer in heavy smokers gave them beta carotene supplements. Results showed the supplements actually increased the risk of cancer in smokers.
• Exercise most days of the week. If you don't exercise regularly, start out slowly. Try to exercise most days of the week.

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Lung cancer

Affiliations.

• 1 Peter MacCallum Cancer Centre, Melbourne, VIC, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, VIC, Australia.
• 2 Department of Medicine, Massachusetts General Hospital, Boston, MA, USA.
• 3 Department of Medicine, Massachusetts General Hospital, Boston, MA, USA. Electronic address: [email protected].
• PMID: 34273294
• DOI: 10.1016/S0140-6736(21)00312-3

Lung cancer is one of the most frequently diagnosed cancers and the leading cause of cancer-related deaths worldwide with an estimated 2 million new cases and 1·76 million deaths per year. Substantial improvements in our understanding of disease biology, application of predictive biomarkers, and refinements in treatment have led to remarkable progress in the past two decades and transformed outcomes for many patients. This seminar provides an overview of advances in the screening, diagnosis, and treatment of non-small-cell lung cancer and small-cell lung cancer, with a particular focus on targeted therapies and immune checkpoint inhibitors.

Copyright © 2021 Elsevier Ltd. All rights reserved.

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• Research Support, Non-U.S. Gov't
• Carcinoma, Non-Small-Cell Lung / diagnosis*
• Carcinoma, Non-Small-Cell Lung / therapy*
• Lung Neoplasms / diagnosis*
• Lung Neoplasms / therapy*
• Small Cell Lung Carcinoma / diagnosis*
• Small Cell Lung Carcinoma / therapy*

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• Published: 21 July 2023

The global burden of lung cancer: current status and future trends

• Amanda Leiter   ORCID: orcid.org/0000-0001-9072-5512 1 ,
• Rajwanth R. Veluswamy 2 , 4 &
• Juan P. Wisnivesky 3  

Nature Reviews Clinical Oncology volume  20 ,  pages 624–639 ( 2023 ) Cite this article

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• Cancer epidemiology
• Health policy
• Non-small-cell lung cancer
• Public health

Lung cancer is the leading cause of cancer-related death worldwide. However, lung cancer incidence and mortality rates differ substantially across the world, reflecting varying patterns of tobacco smoking, exposure to environmental risk factors and genetics. Tobacco smoking is the leading risk factor for lung cancer. Lung cancer incidence largely reflects trends in smoking patterns, which generally vary by sex and economic development. For this reason, tobacco control campaigns are a central part of global strategies designed to reduce lung cancer mortality. Environmental and occupational lung cancer risk factors, such as unprocessed biomass fuels, asbestos, arsenic and radon, can also contribute to lung cancer incidence in certain parts of the world. Over the past decade, large-cohort clinical studies have established that low-dose CT screening reduces lung cancer mortality, largely owing to increased diagnosis and treatment at earlier disease stages. These data have led to recommendations that individuals with a high risk of lung cancer undergo screening in several economically developed countries and increased implementation of screening worldwide. In this Review, we provide an overview of the global epidemiology of lung cancer. Lung cancer risk factors and global risk reduction efforts are also discussed. Finally, we summarize lung cancer screening policies and their implementation worldwide.

Lung cancer is the leading cause of cancer death globally, with incidence and mortality trends varying greatly by country and largely reflecting differences in tobacco smoking trends.

Cigarette smoking is the most prevalent lung cancer risk factor, although environmental exposures, such as biomass fuels, asbestos, arsenic and radon, are all important lung factor risk factors with levels of exposure that vary widely across the globe.

Lung cancer incidence and mortality rates are highest in economically developed countries in which tobacco smoking peaked several decades ago, although these rates have mostly now peaked and are declining.

Reductions in lung cancer mortality in economically developed countries reflect decreased incidence (mirroring declines in tobacco smoking) and improvements in treatment of patients with advanced-stage disease, including immunotherapies and targeted therapies.

In low-income and middle-income countries at the later stages of the tobacco epidemic, both lung cancer incidence and mortality are increasing, thus highlighting the importance of tobacco mitigation policies for reducing the global burden of lung cancer.

Low-dose CT-based lung cancer screening reduces lung cancer mortality, although adoption of lung cancer screening programmes has been slow, with limited uptake compared with other cancer screening programmes.

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Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Amanda Leiter

Division of Hematology and Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Rajwanth R. Veluswamy

Division of General Internal Medicine, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, NY, USA

Juan P. Wisnivesky

Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA

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Correspondence to Amanda Leiter .

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R.V. has acted as an adviser and/or consultant to AstraZeneca, Beigene, BerGenBio, Bristol-Myers Squibb, Merck, Novartis, Novocure and Regeneron, and has received research grants from AstraZeneca, Boehringer Ingelheim, Bristol-Myers Squibb, and Onconova Therapeutics. J.P.W. has acted as an adviser and/or consultant to Atea, Banook, PPD and Sanofi and has received research grants from Arnold Consultants, Regeneron and Sanofi. A.L. declares no competing interests.

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Leiter, A., Veluswamy, R.R. & Wisnivesky, J.P. The global burden of lung cancer: current status and future trends. Nat Rev Clin Oncol 20 , 624–639 (2023). https://doi.org/10.1038/s41571-023-00798-3

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Lung Cancer Research Results and Study Updates

See Advances in Lung Cancer Research for an overview of recent findings and progress, plus ongoing projects supported by NCI.

The results of the clinical trial that led to FDA’s 2023 approval of repotrectinib (Augtyro) for lung cancers with ROS1 fusions have been published. The drug shrank tumors in 80% of people receiving the drug as an initial treatment.

Tarlatamab, a new type of targeted immunotherapy, shrank small cell lung cancer (SCLC) tumors in more than 30% of participants in an early-stage clinical trial. Participants had SCLC that had progressed after previous treatments with other drugs.

For people with lung cancer and medullary thyroid cancer whose tumors have changes in the RET gene, selpercatinib improved progression-free survival compared with other common treatments, according to new clinical trial results.

In the ADAURA clinical trial, people with early-stage lung cancer treated with osimertinib (Tagrisso) after surgery lived longer than people treated with a placebo after surgery. Despite some criticisms about its design, the trial is expected to change patient care.

For certain people with early-stage non-small cell lung cancer, sublobar surgery to remove only a piece of the affected lung lobe is as effective as surgery to remove the whole lobe, new research shows.

Pragmatica-Lung is a clinical trial for people with non-small cell lung cancer that has spread beyond the lungs (stage 4 cancer). The trial will help confirm if the combination of pembrolizumab and ramucirumab helps people with advanced lung cancer live longer.

On August 11, the Food and Drug Administration (FDA) gave accelerated approval to trastuzumab deruxtecan (Enhertu) for adults with non-small cell lung cancer (NSCLC) that has a specific mutation in the HER2 gene. Around 3% of people with NSCLC have this kind of HER2 mutation.

Giving people with early-stage lung cancer the immunotherapy drug nivolumab (Opdivo) and chemotherapy before surgery can substantially delay the progression or return of their cancer, a large clinical trial found.

Atezolizumab (Tecentriq) is now the first immunotherapy approved by FDA for use as an additional, or adjuvant, treatment for some patients with non-small cell lung cancer. The approval was based on results of a clinical trial called IMpower010.

Quitting smoking after a diagnosis of early-stage lung cancer may help people live longer, a new study finds. The study, which included more than 500 patients, also found that quitting smoking delayed the cancer from returning or getting worse.

NCI scientists and their international collaborators have found that the majority of lung cancers in never smokers arise when mutations caused by natural processes in the body accumulate. They also identified three subtypes of lung cancer these individuals.

FDA has approved the first KRAS-blocking drug, sotorasib (Lumakras). The approval, which covers the use of sotorasib to treat some patients with advanced lung cancer, sets the stage for other KRAS inhibitors already in development, researchers said.

Combining the chemotherapy drug topotecan and the investigational drug berzosertib shrank tumors in some patients with small cell lung cancer, results from an NCI-supported phase 1 clinical trial show. Two phase 2 trials of the combination are planned.

Mortality rates from the most common lung cancer, non-small cell lung cancer (NSCLC), have fallen sharply in the United States in recent years, due primarily to recent advances in treatment, an NCI study shows.

In a study of more than 50,000 veterans with lung cancer, those with mental illness who received mental health treatment—including for substance use—lived substantially longer than those who didn’t participate in such programs.

FDA has granted accelerated approval for selpercatinib (Retevmo) to treat certain patients with thyroid cancer or non-small cell lung cancer whose tumors have RET gene alterations. The drug, which works by blocking the activity of RET proteins, was approved based on the results of the LIBRETTO-001 trial.

Osimertinib (Tagrisso) improves survival in people with non-small cell lung cancer with EGFR mutations, updated clinical trial results show. People treated with osimertinib lived longer than those treated with earlier-generation EGFR-targeted drugs.

A large clinical trial showed that adding the immunotherapy drug durvalumab (Imfinzi) to standard chemotherapy can prolong survival in some people with previously untreated advanced small cell lung cancer.

The investigational drug selpercatinib may benefit patients with lung cancer whose tumors have alterations in the RET gene, including fusions with other genes, according to results from a small clinical trial.

FDA has approved entrectinib (Rozlytrek) for the treatment of children and adults with tumors bearing an NTRK gene fusion. The approval also covers adults with non-small cell lung cancer harboring a ROS1 gene fusion.

Clinical recommendations on who should be screened for lung cancer may need to be reviewed when it comes to African Americans who smoke, findings from a new study suggest.

Use of a multipronged approach within hospitals, including community centers, not only eliminated treatment disparities among black and white patients with early-stage lung cancer, it also improved treatment rates for all patients, results from a new study show.

In everyday medical care, there may be more complications from invasive diagnostic procedures performed after lung cancer screening than has been reported in large studies.

The Lung Cancer Master Protocol, or Lung-MAP, is a precision medicine research study for people with advanced non-small cell lung cancer that has continued to grow after treatment. Patients are assigned to different study drug combinations based on the results of genomic profiling of their tumors.

On December 6, 2018, the Food and Drug Administration (FDA) approved atezolizumab (Tecentriq) in combination with a standard three-drug regimen as an initial treatment for advanced lung cancer that does not have EGFR or ALK mutations.

A new study has identified a potential biomarker of early-stage non–small cell lung cancer (NSCLC). The biomarker, the study’s leaders said, could help diagnose precancerous lung growths and early-stage lung cancers noninvasively and distinguish them from noncancerous growths.

Results from two large clinical trials should cement the value of the drugs brigatinib (Alunbrig) and durvalumab (Imfinzi) in treating non-small cell lung cancer (NSCLC). The trial results, several experts said, confirm that the drugs can improve the outcomes of patients with advanced NSCLC.

Cancer researchers have trained a computer program to scan images of tissue samples to differentiate normal lung tissue from the two most common forms of lung cancer. The program also learned to detect cancer-related genetic mutations in the samples.

A collection of material about the ALCHEMIST lung cancer trials that will examine tumor tissue from patients with certain types of early-stage, completely resected non-small cell lung cancer for gene mutations in the EGFR and ALK genes, and assign patients with these gene mutations to treatment trials testing post-surgical use of drugs targeted against these mutations.

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Among terminal diseases humanity has not yet learned to treat, cancer is probably one of the most feared illnesses. Unlike AIDS or other diseases widely spread in countries with low standards of living, cancer’s geography is much wider, including both rich and poor countries equally. Among the variety of different types of cancer, one of the most common is lung cancer; the environment in which people live in the 21st century greatly contributes to the development of this type of cancer.

The first and the most popular cause of lung cancer is smoking cigarettes. By numerous estimates, smoking cigarettes causes approximately 86% of lung cancer cases, including cases caused by passive exposure to smoke exhaled by other smokers. These chances increase if a person started smoking tobacco at a young age. Passive smoking poses a lesser threat, but is still dangerous—it is known that passive smokers (who are usually exposed to smoke at work or at home) have a 25% higher risk of lung cancer compared to people who are not exposed to the smoke of cigarettes. Regular heavy exposure to environmental tobacco smoke can increase the risk of lung cancer by 50% ( National Cancer Institute ).

Genetics and lung diseases in one’s genetics can also become significant risk factors of lung cancer. For example, if a person’s mother, father, sibling, aunt, uncle, or grandparent has had lung cancer, the chances of this person developing lung cancer slightly increases. At the same time, it has not been yet researched whether genes indeed increase cancer chances, or they increase individuals’ susceptibility to this disease. As for lung diseases, some of them are known to affect the chances of cancer development. In particular, among such diseases are tuberculosis and chronic obstructive pulmonary disease. Other illnesses like chronic bronchitis and emphysema can cause scarring in the lungs, which means the increase of the amount of tissue in them—and as it is known, cancer is an uncontrolled division of cells, and the respective multiplication of tissues ( Healthline ).

As for other environmental factors , one of the most significant among them is the exposure to asbestos fibers and similar materials. Usually, a person is exposed to these silicate materials at the workplace: technical works, such as thermal and acoustic insulation, involve the usage of asbestos. Nowadays, asbestos is limited or even prohibited from usage, since it has been proven that asbestos materials can cause both lung cancer and mesothelioma (cancer of the lungs’ pleura, as well as cancer of peritoneum—a lining of the abdominal cavity). Even non-smoking asbestos workers have a five times higher risk of developing lung cancer; as for the smoking asbestos workers, their chances to get cancer are up to ninety-fold greater than nonsmokers ( MedicineNet.com ).

As it can be seen, lung cancer does not develop on its own, but is triggered by a number of factors. The first and foremost of them is smoking tobacco, both active and passive. Exposure to asbestos materials also increases a person’s chances to get lung cancer. Also, genetics and past lung illnesses can lead to the development of this type of cancer. The cure for lung cancer is not finalized, and remains an epidemic.

“Lung Cancer Symptoms, Causes, Treatment.” MedicineNet. N.p., n.d. Web. 12 Aug. 2015.

“Lung Cancer Risks and Causes.” CancerResearch UK. N.p., n.d. Web. 12 Aug. 2015.

“Lung Cancer Causes.” Healthline. N.p., n.d. Web. 12 Aug. 2015.

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Lung Cancer: Introduction

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Lung cancer is now the most prevalent form of cancer affecting Americans with an estimated 222,500 new cases every year, according to the American Cancer Society (ACS, 2010). Beyond being the most common form of cancer, lung cancer is also often difficult to treat. As a result, lung cancer is the most deadly cancer with roughly 160,000 Americans dying from it every year.  This is about 30% of all cancer deaths!  (ACS, 2010).

Although lung cancer is difficult to treat and cure, it is for the most part preventable. Lifestyle choices can be made which can almost eliminate your risk for getting the disease. Your decision to stop smoking and to eat a healthy diet featuring plenty of fresh fruits and vegetables can greatly decrease your risk.

Types Of Lung Cancer

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Lung cancers are broken down into two major types, small cell lung cancer and nonsmall cell lung cancer. The difference between the two types involves where they originate, how fast they grow, and how they are best treated.

Small cell lung cancers comprise roughly 15% of all lung cancer cases (ACS, 2010). This type of lung cancer originates in an inner layer of the walls of the bronchi called the bronchial submucosa, and grows aggressively (in comparison with nonsmall cell lung cancers), quickly spreading into surrounding tissues, and ultimately, through the body. Though the growth of this cancer is rapid, there are few or no clues that anything is particularly amiss. Symptoms are generally not noticeable until the cancer has spread into other parts of the body. Because of their rapid growth pace and tendency to metastasize, small cell cancers are described with only two stages (limited – when spread is contained to the localized area of the lung and immediate surrounding tissues, and extensive – when the cancer has spread throughout the body). By the time patients present for treatment, small cell lung cancers have generally reached their extensive stage. Treatment generally takes the form of a combined chemotherapy and radiation therapy approach.

Non-small cell lung cancers comprise about 85% of all lung cancers and can be broken down into three subtypes; squamous cell carcinoma, adenocarcinoma, and large cell lung cancer (ACS, 2010). Treatment of these types of cancer typically includes a combination of surgery, chemotherapy and radiation therapy. 

• Squamous cell carcinoma most often begins in the larger sections of the bronchi. It progresses slowest of all of the lung cancers.
• Adenocarcinomas have the fastest growing incidence of any type of lung cancer in the United States, reported with frequency in both smokers and persons who never smoked. They typically occur at the periphery of the lungs, and grow more aggressively than squamous cell forms of lung cancer.
• As the name suggests, large cell lung cancers form as clusters of large undifferentiated cells. Like ademocarcinomas, they tend to occur at the periphery of the lung, growing and spreading more aggressively than squamous cell forms of lung cancer.

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Essay on Cancer for Students and Children

500+ words essay on cancer.

Cancer might just be one of the most feared and dreaded diseases. Globally, cancer is responsible for the death of nearly 9.5 million people in 2018. It is the second leading cause of death as per the world health organization. As per studies, in India, we see 1300 deaths due to cancer every day. These statistics are truly astonishing and scary. In the recent few decades, the number of cancer has been increasingly on the rise. So let us take a look at the meaning, causes, and types of cancer in this essay on cancer.

Cancer comes in many forms and types. Cancer is the collective name given to the disease where certain cells of the person’s body start dividing continuously, refusing to stop. These extra cells form when none are needed and they spread into the surrounding tissues and can even form malignant tumors. Cells may break away from such tumors and go and form tumors in other places of the patient’s body.

Types of Cancers

As we know, cancer can actually affect any part or organ of the human body. We all have come across various types of cancer – lung, blood, pancreas, stomach, skin, and so many others. Biologically, however, cancer can be divided into five types specifically – carcinoma, sarcoma, melanoma, lymphoma, leukemia.

Among these, carcinomas are the most diagnosed type. These cancers originate in organs or glands such as lungs, stomach, pancreas, breast, etc. Leukemia is the cancer of the blood, and this does not form any tumors. Sarcomas start in the muscles, bones, tissues or other connective tissues of the body. Lymphomas are the cancer of the white blood cells, i.e. the lymphocytes. And finally, melanoma is when cancer arises in the pigment of the skin.

Get the huge list of more than 500 Essay Topics and Ideas

Causes of Cancer

In most cases, we can never attribute the cause of any cancer to one single factor. The main thing that causes cancer is a substance we know as carcinogens. But how these develop or enters a person’s body will depend on many factors. We can divide the main factors into the following types – biological factors, physical factors, and lifestyle-related factors.

Biological factors involve internal factors such as age, gender, genes, hereditary factors, blood type, skin type, etc. Physical factors refer to environmental exposure of any king to say X-rays, gamma rays, etc. Ad finally lifestyle-related factors refer to substances that introduced carcinogens into our body. These include tobacco, UV radiation, alcohol. smoke, etc. Next, in this essay on cancer lets learn about how we can treat cancer.

Treatment of Cancer

Early diagnosis and immediate medical care in cancer are of utmost importance. When diagnosed in the early stages, then the treatment becomes easier and has more chances of success. The three most common treatment plans are either surgery, radiation therapy or chemotherapy.

If there is a benign tumor, then surgery is performed to remove the mass from the body, hence removing cancer from the body. In radiation therapy, we use radiation (rays) to specially target and kill the cancer cells. Chemotherapy is similar, where we inject the patient with drugs that target and kill the cancer cells. All treatment plans, however, have various side-effects. And aftercare is one of the most important aspects of cancer treatment.

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Abstract 3158: TUSC2 suppresses energy metabolism in lung cancer cells with opposite effects in normal bronchial epithelial cells

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Jane Tonello , Mark Berger , Anil Shanker , Alla Ivanova; Abstract 3158: TUSC2 suppresses energy metabolism in lung cancer cells with opposite effects in normal bronchial epithelial cells. Cancer Res 15 March 2024; 84 (6_Supplement): 3158. https://doi.org/10.1158/1538-7445.AM2024-3158

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Introduction: TUSC2 (TUmor Suppressor Candidate 2) is a tumor suppressor gene from the human 3p21.3 chromosomal region frequently deleted in lung cancers. Independently of deletion, reduced expression of TUSC2 is observed in ~ 80% of lung cancers, mesothelioma, breast, head-and neck, osteosarcoma, glioblastoma, and other cancers, suggesting a critical anti-tumor role of TUSC2. TUSC2 resides in mitochondria and is involved mitochondrial respiration/energy metabolism, ROS production, Ca 2+ flux to/from mitochondria, etc. Studies on tumor-bearing mice treated with TUSC2-containing plasmid encapsulated in lipid nanoparticles (quaratusugene ozeplasmid) and Phase I and II clinical trials of quar oze in lung cancer patients provides a strong rationale to further study the tumor-protective mechanisms of TUSC2 protein. Main scientific question. We asked if and how human lung cancer cells, A549 and H358, that have ~80-90% decrease in TUSC2 expression, change their energy metabolism in response to re-introduction of TUSC2 as compared to Beas2B, a normal bronchial epithelial cell line. Cancer cells rely heavily on anaerobic glycolysis, while normal epithelial cells use mitochondrial respiration as a primary way of energy production.

Methods: Transient transfection of TUSC2-expressing plasmid to 3 cell lines; qPCR to confirm TUSC2 delivery; Seahorse analysis of energy production that measures in real time Oxygen Consumption Rate (OCR) and Extracellular Acidification Rate (ECAR) in different conditions.

Results: All three cell lines demonstrated high transfection efficiency. Seahorse analysis revealed that TUSC2 re-introduction to TUSC2-deficient cancer cells consistently suppressed both glycolytic and mitochondrial ATP production, thus leaving cells without sufficient energy to support their vital functions. We found a significant decrease in basal and maximal respiration, spare respiratory capacity, ATP production, glycolysis and glycolytic capacity in cancer cell lines transfected with TUSC2-expressing plasmid. Unlike cancer cells, both glycolytic and mitochondrial metabolism of normal epithelial cells Beas2B were significantly strengthened after the introduction of TUSC2, suggesting a beneficial role of TUSC2 for the metabolic health of normal cells. The experiments were repeated four times; Student T-test was used to calculate statistical significance.

Therapeutic Significance: These experiments suggest that TUSC2 plasmid delivery to cancer patients, and thus quar oze therapeutic use, may target and disrupt the metabolism of cancer cells, triggering either senescence or apoptotic pathways, while on the other hand, supporting the metabolism of normal epithelial cells. These data have high therapeutic significance, suggesting that one of the anti-tumor mechanisms of quar oze action in patients is the suppression of cancer cell metabolism resulting in cancer cell death.

Citation Format: Jane Tonello, Mark Berger, Anil Shanker, Alla Ivanova. TUSC2 suppresses energy metabolism in lung cancer cells with opposite effects in normal bronchial epithelial cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 3158.

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Office on Smoking and Health (US). The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2006.

The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General.

1 introduction, summary, and conclusions.

• Introduction

The topic of passive or involuntary smoking was first addressed in the 1972 U.S. Surgeon General’s report ( The Health Consequences of Smoking , U.S. Department of Health, Education, and Welfare [USDHEW] 1972 ), only eight years after the first Surgeon General’s report on the health consequences of active smoking ( USDHEW 1964 ). Surgeon General Dr. Jesse Steinfeld had raised concerns about this topic, leading to its inclusion in that report. According to the 1972 report, nonsmokers inhale the mixture of sidestream smoke given off by a smoldering cigarette and mainstream smoke exhaled by a smoker, a mixture now referred to as “secondhand smoke” or “environmental tobacco smoke.” Cited experimental studies showed that smoking in enclosed spaces could lead to high levels of cigarette smoke components in the air. For carbon monoxide ( CO ) specifically, levels in enclosed spaces could exceed levels then permitted in outdoor air. The studies supported a conclusion that “an atmosphere contaminated with tobacco smoke can contribute to the discomfort of many individuals” ( USDHEW 1972 , p. 7). The possibility that CO emitted from cigarettes could harm persons with chronic heart or lung disease was also mentioned.

Secondhand tobacco smoke was then addressed in greater depth in Chapter 4 (Involuntary Smoking) of the 1975 Surgeon General’s report, The Health Consequences of Smoking ( USDHEW 1975 ). The chapter noted that involuntary smoking takes place when nonsmokers inhale both sidestream and exhaled mainstream smoke and that this “smoking” is “involuntary” when “the exposure occurs as an unavoidable consequence of breathing in a smoke-filled environment” (p. 87). The report covered exposures and potential health consequences of involuntary smoking, and the researchers concluded that smoking on buses and airplanes was annoying to nonsmokers and that involuntary smoking had potentially adverse consequences for persons with heart and lung diseases. Two studies on nicotine concentrations in nonsmokers raised concerns about nicotine as a contributing factor to atherosclerotic cardiovascular disease in nonsmokers.

The 1979 Surgeon General’s report, Smoking and Health: A Report of the Surgeon General ( USDHEW 1979 ), also contained a chapter entitled “Involuntary Smoking.” The chapter stressed that “attention to involuntary smoking is of recent vintage, and only limited information regarding the health effects of such exposure upon the nonsmoker is available” (p. 11–35). The chapter concluded with recommendations for research including epidemiologic and clinical studies. The 1982 Surgeon General’s report specifically addressed smoking and cancer ( U.S. Department of Health and Human Services [USDHHS] 1982 ). By 1982, there were three published epidemiologic studies on involuntary smoking and lung cancer, and the 1982 Surgeon General’s report included a brief chapter on this topic. That chapter commented on the methodologic difficulties inherent in such studies, including exposure assessment, the lengthy interval during which exposures are likely to be relevant, and accounting for exposures to other carcinogens. Nonetheless, the report concluded that “Although the currently available evidence is not sufficient to conclude that passive or involuntary smoking causes lung cancer in nonsmokers, the evidence does raise concern about a possible serious public health problem” (p. 251).

Involuntary smoking was also reviewed in the 1984 report, which focused on chronic obstructive pulmonary disease and smoking ( USDHHS 1984 ). Chapter 7 (Passive Smoking) of that report included a comprehensive review of the mounting information on smoking by parents and the effects on respiratory health of their children, data on irritation of the eye, and the more limited evidence on pulmonary effects of involuntary smoking on adults. The chapter began with a compilation of measurements of tobacco smoke components in various indoor environments. The extent of the data had increased substantially since 1972. By 1984, the data included measurements of more specific indicators such as acrolein and nicotine, and less specific indicators such as particulate matter ( PM ), nitrogen oxides, and CO . The report reviewed new evidence on exposures of nonsmokers using bio-markers, with substantial information on levels of cotinine, a major nicotine metabolite. The report anticipated future conclusions with regard to respiratory effects of parental smoking on child respiratory health ( Table 1.1 ).

Conclusions from previous Surgeon General’s reports on the health effects of secondhand smoke exposure

Involuntary smoking was the topic for the entire 1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking ( USDHHS 1986 ). In its 359 pages, the report covered the full breadth of the topic, addressing toxicology and dosimetry of tobacco smoke; the relevant evidence on active smoking; patterns of exposure of nonsmokers to tobacco smoke; the epidemiologic evidence on involuntary smoking and disease risks for infants, children, and adults; and policies to control involuntary exposure to tobacco smoke. That report concluded that involuntary smoking caused lung cancer in lifetime nonsmoking adults and was associated with adverse effects on respiratory health in children. The report also stated that simply separating smokers and nonsmokers within the same airspace reduced but did not eliminate exposure to secondhand smoke. All of these findings are relevant to public health and public policy ( Table 1.1 ). The lung cancer conclusion was based on extensive information already available on the carcinogenicity of active smoking, the qualitative similarities between secondhand and mainstream smoke, the uptake of tobacco smoke components by nonsmokers, and the epidemiologic data on involuntary smoking. The three major conclusions of the report ( Table 1.2 ), led Dr. C. Everett Koop, Surgeon General at the time, to comment in his preface that “the right of smokers to smoke ends where their behavior affects the health and well-being of others; furthermore, it is the smokers’ responsibility to ensure that they do not expose nonsmokers to the potential [ sic ] harmful effects of tobacco smoke” ( USDHHS 1986 , p. xii).

Major conclusions of the 1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking

Two other reports published in 1986 also reached the conclusion that involuntary smoking increased the risk for lung cancer. The International Agency for Research on Cancer ( IARC ) of the World Health Organization concluded that “passive smoking gives rise to some risk of cancer” ( IARC 1986 , p. 314). In its monograph on tobacco smoking, the agency supported this conclusion on the basis of the characteristics of sidestream and mainstream smoke, the absorption of tobacco smoke materials during an involuntary exposure, and the nature of dose-response relationships for carcinogenesis. In the same year, the National Research Council ( NRC ) also concluded that involuntary smoking increases the incidence of lung cancer in nonsmokers ( NRC 1986 ). In reaching this conclusion, the NRC report cited the biologic plausibility of the association between exposure to secondhand smoke and lung cancer and the supporting epidemiologic evidence. On the basis of a pooled analysis of the epidemiologic data adjusted for bias, the report concluded that the best estimate for the excess risk of lung cancer in nonsmokers married to smokers was 25 percent, compared with nonsmokers married to nonsmokers. With regard to the effects of involuntary smoking on children, the NRC report commented on the literature linking secondhand smoke exposures from parental smoking to increased risks for respiratory symptoms and infections and to a slightly diminished rate of lung growth.

Since 1986, the conclusions with regard to both the carcinogenicity of secondhand smoke and the adverse effects of parental smoking on the health of children have been echoed and expanded ( Table 1.3 ). In 1992, the U.S. Environmental Protection Agency ( EPA ) published its risk assessment of secondhand smoke as a carcinogen ( USEPA 1992 ). The agency’s evaluation drew on toxicologic information on secondhand smoke and the extensive literature on active smoking. A comprehensive meta-analysis of the 31 epidemiologic studies of secondhand smoke and lung cancer published up to that time was central to the decision to classify secondhand smoke as a group A carcinogen—namely, a known human carcinogen. Estimates of approximately 3,000 U.S. lung cancer deaths per year in non-smokers were attributed to secondhand smoke. The report also covered other respiratory health effects in children and adults and concluded that involuntary smoking is causally associated with several adverse respiratory effects in children. There was also a quantitative risk assessment for the impact of involuntary smoking on childhood asthma and lower respiratory tract infections in young children.

Selected major reports, other than those of the U.S. Surgeon General, addressing adverse effects from exposure to tobacco smoke

In the decade since the 1992 EPA report, scientific panels continued to evaluate the mounting evidence linking involuntary smoking to adverse health effects ( Table 1.3 ). The most recent was the 2005 report of the California EPA ( Cal/EPA 2005 ). Over time, research has repeatedly affirmed the conclusions of the 1986 Surgeon General’s reports and studies have further identified causal associations of involuntary smoking with diseases and other health disorders. The epidemiologic evidence on involuntary smoking has markedly expanded since 1986, as have the data on exposure to tobacco smoke in the many environments where people spend time. An understanding of the mechanisms by which involuntary smoking causes disease has also deepened.

As part of the environmental health hazard assessment, Cal/EPA identified specific health effects causally associated with exposure to secondhand smoke. The agency estimated the annual excess deaths in the United States that are attributable to secondhand smoke exposure for specific disorders: sudden infant death syndrome ( SIDS ), cardiac-related illnesses (ischemic heart disease), and lung cancer ( Cal/EPA 2005 ). For the excess incidence of other health outcomes, either new estimates were provided or estimates from the 1997 health hazard assessment were used without any revisions ( Cal/EPA 1997 ). Overall, Cal/EPA estimated that about 50,000 excess deaths result annually from exposure to secondhand smoke ( Cal/EPA 2005 ). Estimated annual excess deaths for the total U.S. population are about 3,400 (a range of 3,423 to 8,866) from lung cancer, 46,000 (a range of 22,700 to 69,600) from cardiac-related illnesses, and 430 from SIDS. The agency also estimated that between 24,300 and 71,900 low birth weight or pre-term deliveries, about 202,300 episodes of childhood asthma (new cases and exacerbations), between 150,000 and 300,000 cases of lower respiratory illness in children, and about 789,700 cases of middle ear infections in children occur each year in the United States as a result of exposure to secondhand smoke.

This new 2006 Surgeon General’s report returns to the topic of involuntary smoking. The health effects of involuntary smoking have not received comprehensive coverage in this series of reports since 1986. Reports since then have touched on selected aspects of the topic: the 1994 report on tobacco use among young people ( USDHHS 1994 ), the 1998 report on tobacco use among U.S. racial and ethnic minorities ( USDHHS 1998 ), and the 2001 report on women and smoking ( USDHHS 2001 ). As involuntary smoking remains widespread in the United States and elsewhere, the preparation of this report was motivated by the persistence of involuntary smoking as a public health problem and the need to evaluate the substantial new evidence reported since 1986. This report substantially expands the list of topics that were included in the 1986 report. Additional topics include SIDS , developmental effects, and other reproductive effects; heart disease in adults; and cancer sites beyond the lung. For some associations of involuntary smoking with adverse health effects, only a few studies were reviewed in 1986 (e. g ., ear disease in children); now, the relevant literature is substantial. Consequently, this report uses meta-analysis to quantitatively summarize evidence as appropriate. Following the approach used in the 2004 report ( The Health Consequences of Smoking , USDHHS 2004 ), this 2006 report also systematically evaluates the evidence for causality, judging the extent of the evidence available and then making an inference as to the nature of the association.

Organization of the Report

This twenty-ninth report of the Surgeon General examines the topics of toxicology of secondhand smoke, assessment and prevalence of exposure to secondhand smoke, reproductive and developmental health effects, respiratory effects of exposure to secondhand smoke in children and adults, cancer among adults, cardiovascular diseases, and the control of secondhand smoke exposure.

This introductory chapter (Chapter 1) includes a discussion of the concept of causation and introduces concepts of causality that are used throughout this report; this chapter also summarizes the major conclusions of the report. Chapter 2 (Toxicology of Secondhand Smoke) sets out a foundation for interpreting the observational evidence that is the focus of most of the following chapters. The discussion details the mechanisms that enable tobacco smoke components to injure the respiratory tract and cause nonmalignant and malignant diseases and other adverse effects. Chapter 3 (Assessment of Exposure to Secondhand Smoke) provides a perspective on key factors that determine exposures of people to secondhand smoke in indoor environments, including building designs and operations, atmospheric markers of secondhand smoke, exposure models, and biomarkers of exposure to secondhand smoke. Chapter 4 (Prevalence of Exposure to Secondhand Smoke) summarizes findings that focus on nicotine measurements in the air and cotinine measurements in biologic materials. The chapter includes exposures in the home, workplace, public places, and special populations. Chapter 5 (Reproductive and Developmental Effects from Exposure to Secondhand Smoke) reviews the health effects on reproduction, on infants, and on child development. Chapter 6 (Respiratory Effects in Children from Exposure to Secondhand Smoke) examines the effects of parental smoking on the respiratory health of children. Chapter 7 (Cancer Among Adults from Exposure to Secondhand Smoke) summarizes the evidence on cancer of the lung, breast, nasal sinuses, and the cervix. Chapter 8 (Cardiovascular Diseases from Exposure to Secondhand Smoke) discusses coronary heart disease ( CHD ), stroke, and subclinical vascular disease. Chapter 9 (Respiratory Effects in Adults from Exposure to Secondhand Smoke) examines odor and irritation, respiratory symptoms, lung function, and respiratory diseases such as asthma and chronic obstructive pulmonary disease. Chapter 10 (Control of Secondhand Smoke Exposure) considers measures used to control exposure to secondhand smoke in public places, including legislation, education, and approaches based on building designs and operations. The report concludes with “A Vision for the Future.” Major conclusions of the report were distilled from the chapter conclusions and appear later in this chapter.

Preparation of the Report

This report of the Surgeon General was prepared by the Office on Smoking and Health, National Center for Chronic Disease Prevention and Health Promotion, Coordinating Center for Health Promotion, Centers for Disease Control and Prevention ( CDC ), and U.S. DHHS. Initial chapters were written by 22 experts who were selected because of their knowledge of a particular topic. The contributions of the initial experts were consolidated into 10 major chapters that were then reviewed by more than 40 peer reviewers. The entire manuscript was then sent to more than 30 scientists and experts who reviewed it for its scientific integrity. After each review cycle, the drafts were revised by the scientific editors on the basis of the experts’ comments. Subsequently, the report was reviewed by various institutes and agencies within U.S. DHHS. Publication lags, even short ones, prevent an up-to-the-minute inclusion of all recently published articles and data. Therefore, by the time the public reads this report, there may be additional published studies or data. To provide published information as current as possible, this report includes an Appendix of more recent studies that represent major additions to the literature.

This report is also accompanied by a companion database of key evidence that is accessible through the Internet ( http://www.cdc.gov/tobacco ). The database includes a uniform description of the studies and results on the health effects of exposure to secondhand smoke that were presented in a format compatible with abstraction into standardized tables. Readers of the report may access these data for additional analyses, tables, or figures.

• Definitions and Terminology

The inhalation of tobacco smoke by nonsmokers has been variably referred to as “passive smoking” or “involuntary smoking.” Smokers, of course, also inhale secondhand smoke. Cigarette smoke contains both particles and gases generated by the combustion at high temperatures of tobacco, paper, and additives. The smoke inhaled by nonsmokers that contaminates indoor spaces and outdoor environments has often been referred to as “secondhand smoke” or “environmental tobacco smoke.” This inhaled smoke is the mixture of sidestream smoke released by the smoldering cigarette and the mainstream smoke that is exhaled by a smoker. Sidestream smoke, generated at lower temperatures and under somewhat different combustion conditions than mainstream smoke, tends to have higher concentrations of many of the toxins found in cigarette smoke ( USDHHS 1986 ). However, it is rapidly diluted as it travels away from the burning cigarette.

Secondhand smoke is an inherently dynamic mixture that changes in characteristics and concentration with the time since it was formed and the distance it has traveled. The smoke particles change in size and composition as gaseous components are volatilized and moisture content changes; gaseous elements of secondhand smoke may be adsorbed onto materials, and particle concentrations drop with both dilution in the air or environment and impaction on surfaces, including the lungs or on the body. Because of its dynamic nature, a specific quantitative definition of secondhand smoke cannot be offered.

This report uses the term secondhand smoke in preference to environmental tobacco smoke, even though the latter may have been used more frequently in previous reports. The descriptor “secondhand” captures the involuntary nature of the exposure, while “environmental” does not. This report also refers to the inhalation of secondhand smoke as involuntary smoking, acknowledging that most nonsmokers do not want to inhale tobacco smoke. The exposure of the fetus to tobacco smoke, whether from active smoking by the mother or from her exposure to secondhand smoke, also constitutes involuntary smoking.

• Evidence Evaluation

Following the model of the 1964 report, the Surgeon General’s reports on smoking have included comprehensive compilations of the evidence on the health effects of smoking. The evidence is analyzed to identify causal associations between smoking and disease according to enunciated principles, sometimes referred to as the “Surgeon General’s criteria” or the “Hill” criteria (after Sir Austin Bradford Hill) for causality ( USDHEW 1964 ; USDHHS 2004 ). Application of these criteria involves covering all relevant observational and experimental evidence. The criteria, offered in a brief chapter of the 1964 report entitled “Criteria for Judgment,” included (1) the consistency of the association, (2) the strength of the association, (3) the specificity of the association, (4) the temporal relationship of the association, and (5) the coherence of the association. Although these criteria have been criticized (e. g ., Rothman and Greenland 1998 ), they have proved useful as a framework for interpreting evidence on smoking and other postulated causes of disease, and for judging whether causality can be inferred.

In the 2004 report of the Surgeon General, The Health Consequences of Smoking , the framework for interpreting evidence on smoking and health was revisited in depth for the first time since the 1964 report ( USDHHS 2004 ). The 2004 report provided a four-level hierarchy for interpreting evidence ( Table 1.4 ). The categories acknowledge that evidence can be “suggestive” but not adequate to infer a causal relationship, and also allows for evidence that is “suggestive of no causal relationship.” Since the 2004 report, the individual chapter conclusions have consistently used this four-level hierarchy ( Table 1.4 ), but evidence syntheses and other summary statements may use either the term “increased risk” or “cause” to describe instances in which there is sufficient evidence to conclude that active or involuntary smoking causes a disease or condition. This four-level framework also sharply and completely separates conclusions regarding causality from the implications of such conclusions.

Four-level hierarchy for classifying the strength of causal inferences based on available evidence

That same framework was used in this report on involuntary smoking and health. The criteria dating back to the 1964 Surgeon General’s report remain useful as guidelines for evaluating evidence ( USDHEW 1964 ), but they were not intended to be applied strictly or as a “checklist” that needed to be met before the designation of “causal” could be applied to an association. In fact, for involuntary smoking and health, several of the criteria will not be met for some associations. Specificity, referring to a unique exposure-disease relationship (e. g ., the association between thalidomide use during pregnancy and unusual birth defects), can be set aside as not relevant, as all of the health effects considered in this report have causes other than involuntary smoking. Associations are considered more likely to be causal as the strength of an association increases because competing explanations become less plausible alternatives. However, based on knowledge of dosimetry and mechanisms of injury and disease causation, the risk is anticipated to be only slightly or modestly increased for some associations of involuntary smoking with disease, such as lung cancer, particularly when the very strong relative risks found for active smokers are compared with those for lifetime nonsmokers. The finding of only a small elevation in risk, as in the example of spousal smoking and lung cancer risk in lifetime nonsmokers, does not weigh against a causal association; however, alternative explanations for a risk of a small magnitude need full exploration and cannot be so easily set aside as alternative explanations for a stronger association. Consistency, coherence, and the temporal relationship of involuntary smoking with disease are central to the interpretations in this report. To address coherence, the report draws not only on the evidence for involuntary smoking, but on the even more extensive literature on active smoking and disease.

Although the evidence reviewed in this report comes largely from investigations of secondhand smoke specifically, the larger body of evidence on active smoking is also relevant to many of the associations that were evaluated. The 1986 report found secondhand smoke to be qualitatively similar to mainstream smoke inhaled by the smoker and concluded that secondhand smoke would be expected to have “a toxic and carcinogenic potential that would not be expected to be qualitatively different from that of MS [mainstream smoke]” ( USDHHS 1986 , p. 23). The 2004 report of the Surgeon General revisited the health consequences of active smoking ( USDHHS 2004 ), and the conclusions substantially expanded the list of diseases and conditions caused by smoking. Chapters in the present report consider the evidence on active smoking that is relevant to biologic plausibility for causal associations between involuntary smoking and disease. The reviews included in this report cover evidence identified through search strategies set out in each chapter. Of necessity, the evidence on mechanisms was selectively reviewed. However, an attempt was made to cover all health studies through specified target dates. Because of the substantial amount of time involved in preparing this report, lists of new key references published after these cut-off dates are included in an Appendix . Literature reviews were extended when new evidence was sufficient to possibly change the level of a causal conclusion.

• Major Conclusions

This report returns to involuntary smoking, the topic of the 1986 Surgeon General’s report. Since then, there have been many advances in the research on secondhand smoke, and substantial evidence has been reported over the ensuing 20 years. This report uses the revised language for causal conclusions that was implemented in the 2004 Surgeon General’s report ( USDHHS 2004 ). Each chapter provides a comprehensive review of the evidence, a quantitative synthesis of the evidence if appropriate, and a rigorous assessment of sources of bias that may affect interpretations of the findings. The reviews in this report reaffirm and strengthen the findings of the 1986 report. With regard to the involuntary exposure of nonsmokers to tobacco smoke, the scientific evidence now supports the following major 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 for sudden infant death syndrome ( SIDS ), acute respiratory infections, ear problems, and more severe asthma. Smoking by parents causes respiratory symptoms and slows lung growth in their children.
• Exposure of adults to secondhand smoke has immediate adverse effects on the cardiovascular system and causes coronary heart disease and lung cancer.
• The scientific evidence indicates that there is no risk-free 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 substantial progress in tobacco control.
• Eliminating smoking in indoor spaces fully protects nonsmokers from exposure to secondhand smoke. Separating smokers from nonsmokers, cleaning the air, and ventilating buildings cannot eliminate exposures of nonsmokers to secondhand smoke.
• Chapter Conclusions

Chapter 2 Toxicology of Secondhand Smoke

Evidence of carcinogenic effects from secondhand smoke exposure.

• 1. More than 50 carcinogens have been identified in sidestream and secondhand smoke.
• 2. The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and its condensates and tumors in laboratory animals.
• 3. The evidence is sufficient to infer that exposure of nonsmokers to secondhand smoke causes a significant increase in urinary levels of metabolites of the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ( NNK ). The presence of these metabolites links exposure to secondhand smoke with an increased risk for lung cancer.
• 4. The mechanisms by which secondhand smoke causes lung cancer are probably similar to those observed in smokers. The overall risk of secondhand smoke exposure, compared with active smoking, is diminished by a substantially lower carcinogenic dose.

Mechanisms of Respiratory Tract Injury and Disease Caused by Secondhand Smoke Exposure

• 5. The evidence indicates multiple mechanisms by which secondhand smoke exposure causes injury to the respiratory tract.
• 6. The evidence indicates mechanisms by which secondhand smoke exposure could increase the risk for sudden infant death syndrome.

Mechanisms of Secondhand Smoke Exposure and Heart Disease

• 7. The evidence is sufficient to infer that exposure to secondhand smoke has a prothrombotic effect.
• 8. The evidence is sufficient to infer that exposure to secondhand smoke causes endothelial cell dysfunctions.
• 9. The evidence is sufficient to infer that exposure to secondhand smoke causes atherosclerosis in animal models.

Chapter 3. Assessment of Exposure to Secondhand Smoke

Building designs and operations.

• 1. Current heating, ventilating, and air conditioning systems alone cannot control exposure to secondhand smoke.
• 2. The operation of a heating, ventilating, and air conditioning system can distribute secondhand smoke throughout a building.

Exposure Models

• 3. Atmospheric concentration of nicotine is a sensitive and specific indicator for secondhand smoke.
• 4. Smoking increases indoor particle concentrations.
• 5. Models can be used to estimate concentrations of secondhand smoke.

Biomarkers of Exposure to Secondhand Smoke

• 6. Biomarkers suitable for assessing recent exposures to secondhand smoke are available.
• 7. At this time, cotinine, the primary proximate metabolite of nicotine, remains the biomarker of choice for assessing secondhand smoke exposure.
• 8. Individual biomarkers of exposure to secondhand smoke represent only one component of a complex mixture, and measurements of one marker may not wholly reflect an exposure to other components of concern as a result of involuntary smoking.

Chapter 4. Prevalence of Exposure to Secondhand Smoke

• The evidence is sufficient to infer that large numbers of nonsmokers are still exposed to secondhand smoke.
• Exposure of nonsmokers to secondhand smoke has declined in the United States since the 1986 Surgeon General’s report, The Health Consequences of Involuntary Smoking .
• The evidence indicates that the extent of secondhand smoke exposure varies across the country.
• Homes and workplaces are the predominant locations for exposure to secondhand smoke.
• Exposure to secondhand smoke tends to be greater for persons with lower incomes.
• Exposure to secondhand smoke continues in restaurants, bars, casinos, gaming halls, and vehicles.

Chapter 5. Reproductive and Developmental Effects from Exposure to Secondhand Smoke

• 1. The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke and female fertility or fecundability. No data were found on paternal exposure to secondhand smoke and male fertility or fecundability.

Pregnancy (Spontaneous Abortion and Perinatal Death)

• 2. The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke during pregnancy and spontaneous abortion.

Infant Deaths

• 3. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and neonatal mortality.

Sudden Infant Death Syndrome

• 4. The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and sudden infant death syndrome.

Preterm Delivery

• 5. The evidence is suggestive but not sufficient to infer a causal relationship between maternal exposure to secondhand smoke during pregnancy and preterm delivery.

Low Birth Weight

• 6. The evidence is sufficient to infer a causal relationship between maternal exposure to secondhand smoke during pregnancy and a small reduction in birth weight.

Congenital Malformations

• 7. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and congenital malformations.

Cognitive Development

• 8. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and cognitive functioning among children.

Behavioral Development

• 9. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and behavioral problems among children.

Height/Growth

• 10. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke and children’s height/growth.

Childhood Cancer

• 11. The evidence is suggestive but not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood cancer.
• 12. The evidence is inadequate to infer the presence or absence of a causal relationship between maternal exposure to secondhand smoke during pregnancy and childhood cancer.
• 13. The evidence is inadequate to infer the presence or absence of a causal relationship between exposure to secondhand smoke during infancy and childhood cancer.
• 14. The evidence is suggestive but not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood leukemias.
• 15. The evidence is suggestive but not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood lymphomas.
• 16. The evidence is suggestive but not sufficient to infer a causal relationship between prenatal and postnatal exposure to secondhand smoke and childhood brain tumors.
• 17. The evidence is inadequate to infer the presence or absence of a causal relationship between prenatal and postnatal exposure to secondhand smoke and other childhood cancer types.

Chapter 6. Respiratory Effects in Children from Exposure to Secondhand Smoke

Lower respiratory illnesses in infancy and early childhood.

• 1. The evidence is sufficient to infer a causal relationship between secondhand smoke exposure from parental smoking and lower respiratory illnesses in infants and children.
• 2. The increased risk for lower respiratory illnesses is greatest from smoking by the mother.

Middle Ear Disease and Adenotonsillectomy

• 3. The evidence is sufficient to infer a causal relationship between parental smoking and middle ear disease in children, including acute and recurrent otitis media and chronic middle ear effusion.
• 4. The evidence is suggestive but not sufficient to infer a causal relationship between parental smoking and the natural history of middle ear effusion.
• 5. The evidence is inadequate to infer the presence or absence of a causal relationship between parental smoking and an increase in the risk of adenoidectomy or tonsillectomy among children.

Respiratory Symptoms and Prevalent Asthma in School-Age Children

• 6. The evidence is sufficient to infer a causal relationship between parental smoking and cough, phlegm, wheeze, and breathlessness among children of school age.
• 7. The evidence is sufficient to infer a causal relationship between parental smoking and ever having asthma among children of school age.

Childhood Asthma Onset

• 8. The evidence is sufficient to infer a causal relationship between secondhand smoke exposure from parental smoking and the onset of wheeze illnesses in early childhood.
• 9. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure from parental smoking and the onset of childhood asthma.
• 10. The evidence is inadequate to infer the presence or absence of a causal relationship between parental smoking and the risk of immunoglobulin E-mediated allergy in their children.

Lung Growth and Pulmonary Function

• 11. The evidence is sufficient to infer a causal relationship between maternal smoking during pregnancy and persistent adverse effects on lung function across childhood.
• 12. The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke after birth and a lower level of lung function during childhood.

Chapter 7. Cancer Among Adults from Exposure to Secondhand Smoke

Lung cancer.

• 1. The evidence is sufficient to infer a causal relationship between secondhand smoke exposure and lung cancer among lifetime nonsmokers. This conclusion extends to all secondhand smoke exposure, regardless of location.
• 2. The pooled evidence indicates a 20 to 30 percent increase in the risk of lung cancer from secondhand smoke exposure associated with living with a smoker.

Breast Cancer

• 3. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke and breast cancer.

Nasal Sinus Cavity and Nasopharyngeal Carcinoma

• 4. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and a risk of nasal sinus cancer among nonsmokers.
• 5. The evidence is inadequate to infer the presence or absence of a causal relationship between secondhand smoke exposure and a risk of nasopharyngeal carcinoma among nonsmokers.

Cervical Cancer

• 6. The evidence is inadequate to infer the presence or absence of a causal relationship between secondhand smoke exposure and the risk of cervical cancer among lifetime nonsmokers.

Chapter 8. Cardiovascular Diseases from Exposure to Secondhand Smoke

• The evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality among both men and women.
• Pooled relative risks from meta-analyses indicate a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke.
• The evidence is suggestive but not sufficient to infer a causal relationship between exposure to secondhand smoke and an increased risk of stroke.
• Studies of secondhand smoke and subclinical vascular disease, particularly carotid arterial wall thickening, are suggestive but not sufficient to infer a causal relationship between exposure to secondhand smoke and atherosclerosis.

Chapter 9. Respiratory Effects in Adults from Exposure to Secondhand Smoke

Odor and irritation.

• 1. The evidence is sufficient to infer a causal relationship between secondhand smoke exposure and odor annoyance.
• 2. The evidence is sufficient to infer a causal relationship between secondhand smoke exposure and nasal irritation.
• 3. The evidence is suggestive but not sufficient to conclude that persons with nasal allergies or a history of respiratory illnesses are more susceptible to developing nasal irritation from secondhand smoke exposure.

Respiratory Symptoms

• 4. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among persons with asthma.
• 5. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and acute respiratory symptoms including cough, wheeze, chest tightness, and difficulty breathing among healthy persons.
• 6. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and chronic respiratory symptoms.

Lung Function

• 7. The evidence is suggestive but not sufficient to infer a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in persons with asthma.
• 8. The evidence is inadequate to infer the presence or absence of a causal relationship between short-term secondhand smoke exposure and an acute decline in lung function in healthy persons.
• 9. The evidence is suggestive but not sufficient to infer a causal relationship between chronic secondhand smoke exposure and a small decrement in lung function in the general population.
• 10. The evidence is inadequate to infer the presence or absence of a causal relationship between chronic secondhand smoke exposure and an accelerated decline in lung function.
• 11. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and adult-onset asthma.
• 12. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and a worsening of asthma control.

Chronic Obstructive Pulmonary Disease

• 13. The evidence is suggestive but not sufficient to infer a causal relationship between secondhand smoke exposure and risk for chronic obstructive pulmonary disease.
• 14. The evidence is inadequate to infer the presence or absence of a causal relationship between secondhand smoke exposure and morbidity in persons with chronic obstructive pulmonary disease.

Chapter 10. Control of Secondhand Smoke Exposure

• Workplace smoking restrictions are effective in reducing secondhand smoke exposure.
• Workplace smoking restrictions lead to less smoking among covered workers.
• Establishing smoke-free workplaces is the only effective way to ensure that secondhand smoke exposure does not occur in the workplace.
• The majority of workers in the United States are now covered by smoke-free policies.
• The extent to which workplaces are covered by smoke-free policies varies among worker groups, across states, and by sociodemographic factors. Workplaces related to the entertainment and hospitality industries have notably high potential for secondhand smoke exposure.
• Evidence from peer-reviewed studies shows that smoke-free policies and regulations do not have an adverse economic impact on the hospitality industry.
• Evidence suggests that exposure to secondhand smoke varies by ethnicity and gender.
• In the United States, the home is now becoming the predominant location for exposure of children and adults to secondhand smoke.
• Total bans on indoor smoking in hospitals, restaurants, bars, and offices substantially reduce secondhand smoke exposure, up to several orders of magnitude with incomplete compliance, and with full compliance, exposures are eliminated.
• Exposures of nonsmokers to secondhand smoke cannot be controlled by air cleaning or mechanical air exchange.
• Methodologic Issues

Much of the evidence on the health effects of involuntary smoking comes from observational epidemiologic studies that were carried out to test hypotheses related to secondhand smoke and risk for diseases and other adverse health effects. The challenges faced in carrying out these studies reflect those of observational research generally: assessment of the relevant exposures and outcomes with sufficient validity and precision, selection of an appropriate study design, identification of an appropriate and sufficiently large study population, and collection of information on other relevant factors that may confound or modify the association being studied. The challenge of accurately classifying secondhand smoke exposures confronts all studies of such exposures, and consequently the literature on approaches to and limitations of exposure classification is substantial. Sources of bias that can affect the findings of epidemiologic studies have been widely discussed ( Rothman and Greenland 1998 ), both in general and in relation to studies of involuntary smoking. Concerns about bias apply to any study of an environmental agent and disease risk: misclassification of exposures or outcomes, confounding effect modification, and proper selection of study participants. In addition, the generalizability of findings from one population to another (external validity) further determines the value of evidence from a study. Another methodologic concern affecting secondhand smoke literature comes from the use of meta-analysis to combine the findings of epidemiologic studies; general concerns related to the use of meta-analysis for observational data and more specific concerns related to involuntary smoking have also been raised. This chapter considers these methodologic issues in anticipation of more specific treatment in the following chapters.

Classification of Secondhand Smoke Exposure

For secondhand smoke, as for any environmental factor that may be a cause of disease, the exposure assessment might encompass the time and place of the exposure, cumulative exposures, exposure during a particular time, or a recent exposure ( Jaakkola and Jaakkola 1997 ; Jaakkola and Samet 1999 ). For example, exposures to secondhand smoke across the full life span may be of interest for lung cancer, while only more recent exposures may be relevant to the exacerbation of asthma. For CHD , both temporally remote and current exposures may affect risk. Assessments of exposures are further complicated by the multiplicity of environments where exposures take place and the difficulty of characterizing the exposure in some locations, such as public places or workplaces. Additionally, exposures probably vary qualitatively and quantitatively over time and across locations because of temporal changes and geographic differences in smoking patterns.

Nonetheless, researchers have used a variety of approaches for exposure assessments in epidemiologic studies of adverse health effects from involuntary smoking. Several core concepts that are fundamental to these approaches are illustrated in Figure 1.1 ( Samet and Jaakkola 1999 ). Cigarette smoking is, of course, the source of most secondhand smoke in the United States, followed by pipes, cigars, and other products. Epidemiologic studies generally focus on assessing the exposure, which is the contact with secondhand smoke. The concentrations of secondhand smoke components in a space depend on the number of smokers and the rate at which they are smoking, the volume into which the smoke is distributed, the rate at which the air in the space exchanges with uncontaminated air, and the rate at which the secondhand smoke is removed from the air. Concentration, exposure, and dose differ in their definitions, although the terms are sometimes used without sharp distinctions. However, surrogate indicators that generally describe a source of exposure may also be used to assess the exposure, such as marriage to a smoker or the number of cigarettes smoked in the home. Biomarkers can provide an indication of an exposure or possibly the dose, but for secondhand smoke they are used for recent exposure only.

The determinants of exposure, dose, and biologically effective dose that underlie the development of health effects from smoking. Source: Samet and Jaakkola (more...)

People are exposed to secondhand smoke in a number of different places, often referred to as “microenvironments” ( NRC 1991 ). A microenvironment is a definable location that has a constant concentration of the contaminant of interest, such as secondhand smoke, during the time that a person is there. Some key microenvironments for secondhand smoke include the home, the workplace, public places, and transportation environments ( Klepeis 1999 ). Based on the microenvironmental model, total exposure can be estimated as the weighted average of the concentrations of secondhand smoke or indicator compounds, such as nicotine, in the microenvironments where time is spent; the weights are the time spent in each microenvironment. Klepeis (1999) illustrates the application of the microenvironmental model with national data from the National Human Activity Pattern Survey conducted by the EPA . His calculations yield an overall estimate of exposure to airborne particles from smoking and of the contributions to this exposure from various microenvironments.

Much of the epidemiologic evidence addresses the consequences of an exposure in a particular microenvironment, such as the home (spousal smoking and lung cancer risk or maternal smoking and risk for asthma exacerbation), or the workplace (exacerbation of asthma by the presence of smokers). Some studies have attempted to cover multiple microenvironments and to characterize exposures over time. For example, in the multicenter study of secondhand smoke exposure and lung cancer carried out in the United States, Fontham and colleagues (1994) assessed exposures during childhood, in workplaces, and at home during adulthood. Questionnaires that assess exposures have been the primary tool used in epidemiologic studies of secondhand smoke and disease. Measurement of biomarkers has been added in some studies, either as an additional and complementary exposure assessment approach or for validating questionnaire responses. Some studies have also measured components of secondhand smoke in the air.

Questionnaires generally address sources of exposure in microenvironments and can be tailored to address the time period of interest. Questionnaires represent the only approach that can be used to assess exposures retrospectively over a life span, because available biomarkers only reflect exposures over recent days or, at most, weeks. Questionnaires on secondhand smoke exposure have been assessed for their reliability and validity, generally based on comparisons with either biomarker or air monitoring data as the “gold” standard ( Jaakkola and Jaakkola 1997 ). Two studies evaluated the reliability of questionnaires on lifetime exposures ( Pron et al. 1988 ; Coultas et al. 1989 ). Both showed a high degree of repeatability for questions concerning whether a spouse had smoked, but a lower reliability for responses concerning the quantitative aspects of an exposure. Emerson and colleagues (1995) evaluated the repeatability of information from parents of children with asthma. They found a high reliability for parent-reported tobacco use and for the number of cigarettes to which the child was exposed in the home during the past week.

To assess validity, questionnaire reports of current or recent exposures have been compared with levels of cotinine and other biomarkers. These studies tend to show a moderate correlation between levels of cotinine and questionnaire indicators of exposures ( Kawachi and Colditz 1996 ; Cal/EPA 1997 ; Jaakkola and Jaakkola 1997 ). However, cotinine levels reflect not only exposure but metabolism and excretion ( Benowitz 1999 ). Consequently, exposure is only one determinant of variation in cotinine levels among persons; there also are individual variations in metabolism and excretion rates. In spite of these sources of variability, mean levels of cotinine vary as anticipated across categories of self-reported exposures ( Cal/EPA 1997 ; Jaakkola and Jaakkola 1997 ), and self-reported exposures are moderately associated with measured levels of markers ( Cal/EPA 1997 ; Jaakkola and Jaakkola 1997 ).

Biomarkers are also used for assessing exposures to secondhand smoke. A number of biomarkers are available, but they vary in their specificity and in the dynamics of the temporal relationship between the exposure and the marker level ( Cal/EPA 1997 ; Benowitz 1999 ). These markers include specific tobacco smoke components (nicotine) or metabolites (cotinine and tobacco-specific nitrosamines), nonspecific biomarkers (thiocyanate and CO ), adducts with tobacco smoke components or metabolites (4-amino-biphenyl hemoglobin adducts, benzo[ a ]pyrene DNA adducts, and polycyclic aromatic hydrocarbon albumin adducts), and nonspecific assays (urinary mutagenicity). Cotinine has been the most widely used biomarker, primarily because of its specificity, half-life, and ease of measurement in body fluids (e. g ., urine, blood, and saliva). Biomarkers are discussed in detail in Chapter 3 (Assessment of Exposure to Secondhand Smoke).

Some epidemiologic studies have also incorporated air monitoring, either direct personal sampling or the indirect approach based on the microenvironmental model. Nicotine, present in the gas phase of secondhand smoke, can be monitored passively with a special filter or actively using a pump and a sorbent. Hammond and Leaderer (1987) first described a diffusion monitor for the passive sampling of nicotine in 1987; this device has now been widely used to assess concentrations in different environments and to study health effects. Airborne particles have also been measured using active monitoring devices.

Each of these approaches for assessing exposures has strengths and limitations, and preference for one over another will depend on the research question and its context ( Jaakkola and Jaakkola 1997 ; Jaakkola and Samet 1999 ). Questionnaires can be used to characterize sources of exposures, such as smoking by parents. With air concentrations of markers and time-activity information, estimates of secondhand smoke exposures can be made with the microenvironmental model. Biomarkers provide exposure measures that reflect the patterns of exposure and the kinetics of the marker; the cotinine level in body fluids, for example, reflects an exposure during several days. Air monitoring may be useful for validating measurements of exposure. Exposure assessment strategies are matched to the research question and often employ a mixture of approaches determined by feasibility and cost constraints.

Misclassification of Secondhand Smoke Exposure

Misclassification may occur when classifying exposures, outcomes, confounding factors, or modifying factors. Misclassification may be differential on either exposure or outcome, or it may be random ( Armstrong et al. 1992 ). Differential or nonrandom misclassification may either increase or decrease estimates of effect, while random misclassification tends to reduce the apparent effect and weaken the relationship of exposure with disease risk. In studies of secondhand smoke and disease risk, exposure misclassification has been a major consideration in the interpretation of the evidence, although misclassification of health outcome measures has not been a substantial issue in this research. The consequences for epidemiologic studies of misclassification in general are well established ( Rothman and Greenland 1998 ).

An extensive body of literature on the classification of exposures to secondhand smoke is reviewed in this and other chapters, as well as in some publications on the consequences of misclassification ( Wu 1999 ). Two general patterns of exposure misclassification are of concern to secondhand smoke: (1) random misclassification that is not differential by the presence or absence of the health outcome and (2) systematic misclassification that is differential by the health outcome. In studying the health effects of secondhand smoke in adults, there is a further concern as to the classification of the active smoking status (never, current, or former smoking); in studies of children, the accuracy of secondhand smoke exposure classification is the primary methodologic issue around exposure assessment, but unreported active smoking by adolescents is also a concern.

With regard to random misclassification of secondhand smoke exposures, there is an inherent degree of unavoidable measurement error in the exposure measures used in epidemiologic studies. Questionnaires generally assess contact with sources of an exposure (e. g ., smoking in the home or work-place) and cannot capture all exposures nor the intensity of exposures; biomarkers provide an exposure index for a particular time window and have intrinsic variability. Some building-related factors that determine an exposure cannot be assessed accurately by a questionnaire, such as the rate of air exchange and the size of the microenvironment where time is spent, nor can concentrations be assessed accurately by subjective reports of the perceived level of tobacco smoke. In general, random misclassification of exposures tends to reduce the likelihood that studies of secondhand smoke exposure will find an effect. This type of misclassification lessens the contrast between exposure groups, because some truly exposed persons are placed in the unexposed group and some truly unexposed persons are placed in the exposed group. Differential misclassification, also a concern, may increase or decrease associations, depending on the pattern of misreporting.

One particular form of misclassification has been raised with regard to secondhand smoke exposure and lung cancer: the classification of some current or former smokers as lifetime nonsmokers ( USEPA 1992 ; Lee and Forey 1995 ; Hackshaw et al. 1997 ; Wu 1999 ). The resulting bias would tend to increase the apparent association of secondhand smoke with lung cancer, if the misclassified active smokers are also more likely to be classified as involuntary smokers. Most studies of lung cancer and secondhand smoke have used spousal smoking as a main exposure variable. As smoking tends to aggregate between spouses (smokers are more likely to marry smokers), misclassification of active smoking would tend to be differential on the basis of spousal smoking (the exposure under investigation). Because active smoking is strongly associated with increased disease risk, greater misclassification of an actively smoking spouse as a non-smoker among spouses of smokers compared with spouses of nonsmokers would lead to risk estimates for spousal smoking that are biased upward by the effect of active smoking. This type of misclassification is also relevant to studies of spousal exposure and CHD risk or other diseases also caused by active smoking, although the potential for bias is less because the association of active smoking with CHD is not as strong as with lung cancer.

There have been a number of publications on this form of misclassification. Wu (1999) provides a review, and Lee and colleagues (2001) offer an assessment of potential consequences. A number of models have been developed to assess the extent of bias resulting from the misclassification of active smokers as lifetime nonsmokers ( USEPA 1992 ; Hackshaw et al. 1997 ). These models incorporate estimates of the rate of misclassification, the degree of aggregation of smokers by marriage, the prevalence of smoking in the population, and the risk of lung cancer in misclassified smokers ( Wu 1999 ). Although debate about this issue continues, analyses show that estimates of upward bias from misclassifying active smokers as lifetime nonsmokers cannot fully explain the observed increase in risk for lung cancer among lifetime non-smokers married to smokers ( Hackshaw et al. 1997 ; Wu 1999 ).

There is one additional issue related to exposure misclassification. During the time the epidemiologic studies of secondhand smoke have been carried out, exposure has been widespread and almost unavoidable. Therefore, the risk estimates may be biased downward because there are no truly unexposed persons. The 1986 Surgeon General’s report recognized this methodologic issue and noted the need for further data on population exposures to secondhand smoke ( USDHHS 1986 ). This bias was also recognized in the 1986 report of the NRC , and an adjustment for this misclassification was made to the lung cancer estimate ( NRC 1986 ). Similarly, the 1992 report of the EPA commented on background exposure and made an adjustment ( USEPA 1992 ). Some later studies have attempted to address this issue; for example, in a case-control study of active and involuntary smoking and breast cancer in Switzerland, Morabia and colleagues (2000) used a questionnaire to assess exposure and identified a small group of lifetime nonsmokers who also reported no exposure to secondhand smoke. With this subgroup of controls as the reference population, the risks of secondhand smoke exposure were substantially greater for active smoking than when the full control population was used.

This Surgeon General’s report further addresses specific issues of exposure misclassification when they are relevant to the health outcome under consideration.

Use of Meta-Analysis

Meta-analysis refers to the process of evaluating and combining a body of research literature that addresses a common question. Meta-analysis is composed of qualitative and quantitative components. The qualitative component involves the systematic identification of all relevant investigations, a systematic assessment of their characteristics and quality, and the decision to include or exclude studies based on predetermined criteria. Consideration can be directed toward sources of bias that might affect the findings. The quantitative component involves the calculation and display of study results on common scales and, if appropriate, the statistical combination of these results across studies and an exploration of the reasons for any heterogeneity of findings. Viewing the findings of all studies as a single plot provides insights into the consistency of results and the precision of the studies considered. Most meta-analyses are based on published summary results, although they are most powerful when applied to data at the level of individual participants. Meta-analysis is most widely used to synthesize evidence from randomized clinical trials, sometimes yielding findings that were not evident from the results of individual studies. Meta-analysis also has been used extensively to examine bodies of observational evidence.

Beginning with the 1986 NRC report, meta-analysis has been used to summarize the evidence on involuntary smoking and health. Meta-analysis was central to the 1992 EPA risk assessment of secondhand smoke, and a series of meta-analyses supported the conclusions of the 1998 report of the Scientific Committee on Tobacco and Health in the United Kingdom. The central role of meta-analysis in interpreting and applying the evidence related to involuntary smoking and disease has led to focused criticisms of the use of meta-analysis in this context. Several papers that acknowledged support from the tobacco industry have addressed the epidemiologic findings for lung cancer, including the selection and quality of the studies, the methods for meta-analysis, and dose-response associations ( Fleiss and Gross 1991 ; Tweedie and Mengersen 1995 ; Lee 1998 , 1999 ). In a lawsuit brought by the tobacco industry against the EPA, the 1998 decision handed down by Judge William L . Osteen, Sr., in the North Carolina Federal District Court criticized the approach EPA had used to select studies for its meta-analysis and criticized the use of 90 percent rather than 95 percent confidence intervals for the summary estimates ( Flue-Cured Tobacco Cooperative Stabilization Corp. v. United States Environmental Protection Agency , 857 F. Supp. 1137 [M.D.N.C. 1993]). In December 2002, the 4th U.S. Circuit Court of Appeals threw out the lawsuit on the basis that tobacco companies cannot sue the EPA over its secondhand smoke report because the report was not a final agency action and therefore not subject to court review ( Flue-Cured Tobacco Cooperative Stabilization Corp. v. The United States Environmental Protection Agency , No. 98–2407 [4th Cir., December 11, 2002], cited in 17.7 TPLR 2.472 [2003]).

Recognizing that there is still an active discussion around the use of meta-analysis to pool data from observational studies (versus clinical trials), the authors of this Surgeon General’s report used this methodology to summarize the available data when deemed appropriate and useful, even while recognizing that the uncertainty around the meta-analytic estimates may exceed the uncertainty indicated by conventional statistical indices, because of biases either within the observational studies or produced by the manner of their selection. However, a decision to not combine estimates might have produced conclusions that are far more uncertain than the data warrant because the review would have focused on individual study results without considering their overall pattern, and without allowing for a full accounting of different sample sizes and effect estimates.

The possibility of publication bias has been raised as a potential limitation to the interpretation of evidence on involuntary smoking and disease in general, and on lung cancer and secondhand smoke exposure specifically. A 1988 paper by Vandenbroucke used a descriptive approach, called a “funnel plot,” to assess the possibility that publication bias affected the 13 studies considered in a review by Wald and colleagues (1986) . This type of plot characterizes the relationship between the magnitude of estimates and their precision. Vandenbroucke suggested the possibility of publication bias only in reference to the studies of men. Bero and colleagues (1994) concluded that there had not been a publication bias against studies with statistically significant findings, nor against the publication of studies with nonsignificant or mixed findings in the research literature. The researchers were able to identify only five unpublished “negative” studies, of which two were dissertations that tend to be delayed in publication. A subsequent study by Misakian and Bero (1998) did find a delay in the publication of studies with nonsignificant results in comparison with studies having significant results; whether this pattern has varied over the several decades of research on secondhand smoke was not addressed. More recently, Copas and Shi (2000) assessed the 37 studies considered in the meta-analysis by Hackshaw and colleagues (1997) for publication bias. Copas and Shi (2000) found a significant correlation between the estimated risk of exposure and sample size, such that smaller studies tended to have higher values. This pattern suggests the possibility of publication bias. However, using a funnel plot of the same studies, Lubin (1999) found little evidence for publication bias.

On this issue of publication bias, it is critical to distinguish between indirect statistical arguments and arguments based on actual identification of previously unidentified research. The strongest case against substantive publication bias has been made by researchers who mounted intensive efforts to find the possibly missing studies; these efforts have yielded little nothing that would alter published conclusions ( Bero et al. 1994 ; Glantz 2000 ). Presumably because this exposure is a great public health concern, the findings of studies that do not have statistically significant outcomes continue to be published ( Kawachi and Colditz 1996 ).

The quantitative results of the meta-analyses, however, were not determinate in making causal inferences in this Surgeon General’s report. In particular, the level of statistical significance of estimates from the meta-analyses was not a predominant factor in making a causal conclusion. For that purpose, this report relied on the approach and criteria set out in the 1964 and 2004 reports of the Surgeon General, which involved judgments based on an array of quantitative and qualitative considerations that included the degree of heterogeneity in the designs of the studies that were examined. Sometimes this heterogeneity limits the inference from meta-analysis by weakening the rationale for pooling the study results. However, the availability of consistent evidence from heterogenous designs can strengthen the meta-analytic findings by making it unlikely that a common bias could persist across different study designs and populations.

Confounding

Confounding, which refers in this context to the mixing of the effect of another factor with that of secondhand smoke, has been proposed as an explanation for associations of secondhand smoke with adverse health consequences. Confounding occurs when the factor of interest (secondhand smoke) is associated in the data under consideration with another factor (the confounder) that, by itself, increases the risk for the disease ( Rothman and Greenland 1998 ). Correlates of secondhand smoke exposures are not confounding factors unless an exposure to them increases the risk of disease. A factor proposed as a potential confounder is not necessarily an actual confounder unless it fulfills the two elements of the definition. Although lengthy lists of potential confounding factors have been offered as alternatives to direct associations of secondhand smoke exposures with the risk for disease, the factors on these lists generally have not been shown to be confounding in the particular data of interest.

The term confounding also conveys an implicit conceptualization as to the causal pathways that link secondhand smoke and the confounding factor to disease risk. Confounding implies that the confounding factor has an effect on risk that is independent of secondhand smoke exposure. Some factors considered as potential confounders may, however, be in the same causal pathway as a secondhand smoke exposure. Although socioeconomic status ( SES ) is often cited as a potential confounding factor, it may not have an independent effect but can affect disease risk through its association with secondhand smoke exposure ( Figure 1.2 ). This figure shows general alternative relationships among SES, secondhand smoke exposure, and risk for an adverse effect. SES may have a direct effect, or it may indirectly exert its effect through an association with secondhand smoke exposure, or it may confound the relationship between secondhand smoke exposure and disease risk. To control for SES as a potential confounding factor without considering underlying relationships may lead to incorrect risk estimates. For example, controlling for SES would not be appropriate if it is a determinant of secondhand smoke exposure but has no direct effect.

Model for socioeconomic status (SES) and secondhand smoke (SHS) exposure. Arrows indicate directionality of association.

Nonetheless, because the health effects of involuntary smoking have other causes, the possibility of confounding needs careful exploration when assessing associations of secondhand smoke exposure with adverse health effects. In addition, survey data from the last several decades show that secondhand smoke exposure is associated with correlates of lifestyle that may influence the risk for some health effects, thus increasing concerns for the possibility of confounding ( Kawachi and Colditz 1996 ). Survey data from the United States ( Matanoski et al. 1995 ) and the United Kingdom ( Thornton et al. 1994 ) show that adults with secondhand smoke exposures generally tend to have less healthful lifestyles. However, the extent to which these patterns of association can be generalized, either to other countries or to the past, is uncertain.

The potential bias from confounding varies with the association of the confounder to secondhand smoke exposures in a particular study and to the strength of the confounder as a risk factor. The importance of confounding to the interpretation of evidence depends further on the magnitude of the effect of secondhand smoke on disease. As the strength of an association lessens, confounding as an alternative explanation for an association becomes an increasing concern. In prior reviews, confounding has been addressed either quantitatively ( Hackshaw et al. 1997 ) or qualitatively ( Cal/EPA 1997 ; Thun et al. 1999 ). In the chapters in this report that focus on specific diseases, confounding is specifically addressed in the context of potential confounding factors for the particular diseases.

• Tobacco Industry Activities

The evidence on secondhand smoke and disease risk, given the public health and public policy implications, has been reviewed extensively in the published peer-reviewed literature and in evaluations by a number of expert panels. In addition, the evidence has been criticized repeatedly by the tobacco industry and its consultants in venues that have included the peer-reviewed literature, public meetings and hearings, and scientific symposia that included symposia sponsored by the industry. Open criticism in the peer-reviewed literature can strengthen the credibility of scientific evidence by challenging researchers to consider the arguments proposed by critics and to rebut them.

Industry documents indicate that the tobacco industry has engaged in widespread activities, however, that have gone beyond the bounds of accepted scientific practice ( Glantz 1996 ; Ong and Glantz 2000 , 2001 ; Rampton and Stauber 2000 ; Yach and Bialous 2001 ; Hong and Bero 2002 ; Diethelm et al. 2004 ). Through a variety of organized tactics, the industry has attempted to undermine the credibility of the scientific evidence on secondhand smoke. The industry has funded or carried out research that has been judged to be biased, supported scientists to generate letters to editors that criticized research publications, attempted to undermine the findings of key studies, assisted in establishing a scientific society with a journal, and attempted to sustain controversy even as the scientific community reached consensus ( Garne et al. 2005 ). These tactics are not a topic of this report, but to the extent that the scientific literature has been distorted, they are addressed as the evidence is reviewed. This report does not specifically identify tobacco industry sponsorship of publications unless that information is relevant to the interpretation of the findings and conclusions.

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