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Office of the Surgeon General (US). Eliminating Tobacco-Related Disease and Death: Addressing Disparities: A Report of the Surgeon General [Internet]. Washington (DC): US Department of Health and Human Services; 2024.

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Eliminating Tobacco-Related Disease and Death: Addressing Disparities: A Report of the Surgeon General [Internet].

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Chapter 6Disparities in Smoking-Caused Disease Outcomes and Smoking-Attributable Mortality

Introduction

According to the 2014 Surgeon General’s report, more than 20 million Americans died as a result of smoking or exposure to secondhand tobacco smoke in the 50 years since the first Surgeon General’s report was released in 1964 (U.S. Department of Health and Human Services [USDHHS] 2014). The 2014 Surgeon General’s report showed that smoking impacts nearly every organ of the body (USDHHS 2014). Smoking is causally associated with 12 cancers and is the leading cause of lung cancer, which is the largest cause of cancer deaths in the United States (USDHHS 2014; Cronin et al. 2022). In addition, smoking is a major contributor to incidence and mortality from cardiovascular disease (including coronary heart disease, stroke, congestive heart failure, coronary artery disease, and peripheral arterial disease) and chronic obstructive pulmonary disease (COPD; including chronic bronchitis and emphysema) (USDHHS 2014; Tsao et al. 2023; Centers for Disease Control and Prevention [CDC] n.d.b). Exposure to secondhand tobacco smoke causes lung cancer, coronary heart disease and stroke (USDHHS 2014).

The current report fills critical gaps by describing disparities in incidence and mortality due to smoking-caused diseases including cancer, COPD, and cardiovascular disease, and in smoking- and secondhand tobacco smoke-attributable mortality using various analytic and modeling techniques. This chapter begins by providing a brief overview of differences in select smoking-related health outcomes by sociodemographic characteristics, using the latest available published reports. Modeling is also used to conduct a comprehensive analysis of recent trends and disparities in smoking-attributable mortality by sex and age, race and ethnicity, educational attainment, geographic region, and urbanicity (urban versus rural residency). Data from multiple sources are used to estimate the number of deaths caused by cigarette smoking and exposure to secondhand tobacco smoke in the United States overall and by race and ethnicity. Data sources include the American Community Survey, the National Health Interview Survey (NHIS), the National Health and Nutrition Examination Survey (NHANES), the linked NHIS-National Death Index (NHIS-NDI), the National Vital Statistics System Multiple Cause of Death file, and National Center for Health Statistics’ National Vital Statistics Reports.

The chapter also reviews the findings from various simulation models which are important tools to project the potential effects of large-scale interventions on smoking-attributable morbidity and mortality and on disparities in tobacco use. The chapter concludes with a discussion about gaps in data and research that can be used to further assess the health impacts of tobacco-related health disparities.

Conclusions from Previous Surgeon General’s Reports

The 1998 Surgeon General’s report was the first to focus exclusively on tobacco use and health outcomes among members of four racial and ethnic population groups. That report concluded that cigarette smoking is a major cause of disease in African American, American Indian and Alaska Native, Asian American and Pacific Islander, and Hispanic people; African American people experienced the greatest health burden from cigarette smoking; and lung cancer is the leading cause of cancer deaths for each of the aforementioned racial and ethnic groups (USDHHS 1998).

The 2014 Surgeon General’s report provided a comprehensive review of the health consequences of smoking and reflected on 50 years of progress in tobacco prevention and control. The 2014 Surgeon General’s report acknowledged that tobacco use causes or worsens cardiovascular diseases, diabetes, eye diseases, pneumonia, COPD, tuberculosis, periodontitis, adverse reproductive health outcomes, congenital defects, hip fractures, rheumatoid arthritis, male sexual dysfunction, and immune dysfunction and diminishes overall health (USDHHS 2014). Additionally, exposure to secondhand tobacco smoke causes lung cancer, stroke, cardiovascular disease, adverse reproductive health outcomes, middle ear disease, impaired lung function, lower respiratory illness, and sudden infant death syndrome (USDHHS 2014). Lower relative risks (RRs) for smoking in women than men in earlier studies reflected historical differences in population-level smoking patterns. However, by the 1960s, smoking patterns had largely converged for men and women and by the 21st century, the disease risks from smoking for women are now similar to those of men for lung cancer, COPD, and cardiovascular disease. The 2014 report also concluded that very large disparities in tobacco use remain across groups defined by race, ethnicity, level of educational attainment, socioeconomic status (SES), and geographic region.

A major conclusion of the 2020 Surgeon General’s report on tobacco cessation was that smoking cessation is beneficial at any age (USDHHS 2020). The 2020 report showed that quitting smoking reduces the risk of premature death and the risk of 12 types of cancer compared with continued smoking. It also concluded that disparities in the prevalence of smoking persist, aligning with the conclusions of the 2014 Surgeon General’s report. The 2020 Surgeon General’s report also identified disparities in key indicators of smoking cessation, including quit attempts, having received advice to quit smoking from a health professional, and using counseling and medications to facilitate quitting (USDHHS 2020). As described in Chapter 2 of the present report, the prevalence of smoking is higher among some population groups than it is among others in the United States. Furthermore, cessation behaviors, such as quit attempts, are lower among some groups than among other groups based on level of educational attainment, poverty status, age, health insurance status, race and ethnicity, and geographic region.

Differences in Smoking-Caused Diseases Across Population Groups

The 2010 and 2014 Surgeon General’s reports outlined the biologic mechanisms linking active smoking and exposure to secondhand tobacco smoke with cancer, COPD, cardiovascular disease, and other conditions (USDHHS 2010, 2014). Substantial declines in the prevalence of smoking contributed to a 46.4% decline in the age-standardized rate of years of life lost (YLL) due to premature death associated with smoking from 1990 to 2019, although smoking remained the leading risk factor for YLL during this period (Tsao et al. 2023). Smoking was also the leading risk factor for years of life lived with disability or injury (YLD) in 1990. However, the age-standardized YLD rate attributable to smoking declined by 25.8% from 1990 to 2019, such that smoking ranked as the third most common risk factor for YLD in 2019 (Tsao et al. 2023).

This section provides a brief overview of differences in select smoking-related outcomes by sociodemographic characteristics, using data from the latest available published reports. Consistent with Chapter 2 of this report, differences in select outcomes by sociodemographic characteristics are reported where 95% confidence intervals (CIs) do not overlap, when applicable.

Cancer

Smoking is a causal factor for at least 12 cancers, including cancers of the oropharynx, larynx, esophagus, lung, bronchus and trachea, stomach, liver, pancreas, kidney and ureter, cervix, bladder, colon, and rectum (USDHHS 2014). It is also a causal factor in acute myeloid leukemia (USDHHS 2014). The National Cancer Institute (NCI), the American Association for Cancer Research, the American Cancer Society, and the CDC have published multiple reports that describe overall cancer disparities (Singh et al. 2003; American Association for Cancer Research 2022; Cronin et al. 2022; American Cancer Society n.d.).

Cancer disparities are defined as differences in cancer measures, such as cancer incidence, prevalence, and survival; morbidity and mortality; survivorship (i.e., experiences and challenges resulting from cancer diagnosis); quality of life after cancer treatment; and the burden of cancer or such related conditions as financial costs, screening rates, and stage of diagnosis (International Agency for Research on Cancer 2012; Cancer.Net 2021; NCI 2022).

Consistent socioeconomic disparities in cancer incidence, mortality, and stage of diagnosis have been observed in the United States, particularly for cancers with a high smoking-attributable burden, such as those of the lung, cervix, stomach, and liver (Singh et al. 2003, 2004; Clegg et al. 2009; Du et al. 2011; Singh and Jemal 2017; Withrow et al. 2021). These disparities have been observed among White, Black, Hispanic, Asian and Pacific Islander, and American Indian and Alaska Native people (Singh et al. 2003, 2004; Singh and Jemal 2017). The remainder of this section summarizes key findings on cancer incidence (diagnosed from 2001 to 2018) and mortality (from 2001 to 2019) by sex and race and ethnicity as presented in the most recent Annual Report to the Nation on the Status of Cancer (Cronin et al. 2022). Data for other indicators, such as survival rates and stage of diagnosis by the intersection of race and ethnicity with other sociodemographic factors, are often difficult to report due to small sample sizes.

Cronin and colleagues (2022) presented age-standardized, overall cancer incidence rates (pooled across a fixed 5-year interval from 2014 to 2018) and death rates (pooled across a fixed 5-year interval from 2015 to 2019). Rates were adjusted for delays in the time between diagnosis and reporting to the cancer registry. Rates were presented overall and by sex and race and ethnicity. Race and ethnicity were categorized into five mutually exclusive racial and ethnic groups: non-Hispanic White, non-Hispanic Black, non-Hispanic American Indian and Alaska Native, non-Hispanic Asian and Pacific Islander, and Hispanic. Data on race and ethnicity were abstracted from information reported in medical records (for incident cases) or on death certificates (for deaths). Information was not available for disaggregated racial and ethnic population groups. Hispanic people could be of any race and thus, for brevity, these population groups are referred to as White, Black, American Indian and Alaska Native, Asian and Pacific Islander, and Hispanic.

Additionally, Cronin and colleagues (2022) presented temporal trends in delay-adjusted incidence and death rates from joinpoint regression analyses, allowing for up to three joinpoints for incidence (across a 17-year period from 2001 to 2018) and death (across an 18-year period from 2001 to 2019) rates. The line segments resulting from the joinpoint analyses were reported as the annual percent change (APC). The average APC (AAPC) was presented as the weighted average of the APC over the most recent fixed 5-year interval (incidence: 2014–2018; death: 2015–2019). Statistically significant (p <0.05) temporal trends in the APC or AAPC were considered increasing when the slope was greater than 0 or decreasing when the slope was less than 0. Otherwise, the slope was considered stable. See Cronin and colleagues (2022) for a complete description of the data sources and methodology.

Cancer Incidence Rates

Among men from 2001 to 2018, joinpoint trend analysis found that overall cancer incidence rates were stable from 2001 to 2007, declined by an average of 2.1% per year from 2007 to 2013, and stabilized again from 2013 to 2018. Among women, overall cancer incidence rates were stable from 2001 to 2003 and increased slightly (by about 0.2% per year) from 2003 to 2018. The overall age-adjusted cancer incidence rate during 2014–2018 was 457.5 per 100,000 population; rates were higher rates among men (497.4 per 100,000 population) than among women (430.9 per 100,000 population) (Cronin et al. 2022).

Among the 18 most common sites for cancer for which incidence rates are reported in the Annual Report to the Nation on the Status of Cancer by Cronin and colleagues (2022), more than half were identified in the 2014 Surgeon General’s report as being causally associated with smoking: lung and bronchus, colon and rectum, urinary bladder, kidney and renal pelvis, oral cavity and pharynx, pancreas, liver and intrahepatic bile duct, stomach, esophagus, larynx, and cervix (USDHHS 2014). The incidence of cancers that have been causally associated with smoking have largely declined over time, coinciding with declines in the prevalence of smoking (see Chapter 2). However, the smoking-attributable burden differs by cancer site such that the presence of other risk factors (e.g., alcohol consumption or obesity) may contribute to changing trends. This section describes trends in incidence rates for cancers that have been causally associated with smoking.

Among men during 2014–2018, the incidence of pancreatic (AAPC = 1.1%) and kidney (AAPC = 0.7%) cancers increased. Incidence decreased for cancers of the lung and bronchus (AAPC = −2.6%), larynx (AAPC = −2.4%), bladder (AAPC = −2.1%), stomach (AAPC = −1.8%), and colon and rectum (AAPC = −1.2%). From 2014 to 2018, the incidence of liver, esophageal, and oral cavity and pharyngeal cancers was stable.

Among women during 2014–2018, incidence of cancers of the liver (AAPC = 1.6%), kidney (AAPC = 1.2%), pancreas (AAPC = 1.0%), and oral cavity and pharynx (AAPC = 0.5%) increased. Incidence decreased for cancers of the lung and bronchus (AAPC = −1.1%), colon and rectum (AAPC = −1.2%), and bladder (AAPC = −0.9%). During this period, incidence was stable for cervical and stomach cancers.

During 2014–2018, cancers of the lung and bronchus were the second most common types of cancer diagnosed among men (66.1 per 100,000 population, behind prostate cancer) and women (51.0 per 100,000 population, behind breast cancer). By race and ethnicity, statistically significant declines in lung and bronchus cancers were observed across men of all races and ethnicities and among White, Black, and Hispanic women.

Among men, incidence of lung and bronchus cancers was higher among Black men (78.3 per 100,000 population) than among American Indian and Alaska Native men (73.0 per 100,000 population), White men (70.0 per 100,000 population), Asian and Pacific Islander men (43.3 per 100,000 population), and Hispanic men (34.9 per 100,000 population). During this 5-year fixed interval, the steepest decreasing trends in lung and bronchus cancers were observed among American Indian and Alaska Native men (−5.3% per year) and Black men (−3.2% per year) followed by White men (−2.8% per year), Hispanic men (−2.7% per year), and Asian and Pacific Islander men (−1.5% per year).

Among women, incidence of lung and bronchus cancers was higher among American Indian and Alaska Native women (61.5 per 100,000 population) than it was among White women (56.8 per 100,000 population), Black women (47.8 per 100,000 population), Asian and Pacific Islander women (28.6 per 100,000 population), and Hispanic women (23.1 per 100,000 population). During this 5-year fixed interval, the steepest decreasing trend in lung and bronchus cancers was observed among Black women (−1.6% per year), followed by White women (−0.8% per year) and Hispanic women (−0.7% per year). No significant changes were observed for Asian and Pacific Islander women and American Indian and Alaska Native women.

For a few cancers, the directionality of the trend in incidence from 2014 to 2018 was consistent across all racial and ethnic population groups of men, including the declines in lung and bronchus cancer and stomach cancer, and the increase in pancreatic cancer. For some other cancers, the trends were mostly consistent, but for some racial or ethnic population groups, the trend did not reach statistical significance (such as the decreases in colon and rectum cancer and laryngeal cancer among men).

However, the directionality of trends in cancer incidence were not always consistent across racial and ethnic groups. In some cases, the overall result hid significant changes among some populations. For example, the incidence of esophageal cancer in men did not change significantly overall, but significant decreases were observed for Black, Hispanic, and Asian and Pacific Islander men. Results for some cancers were discordant across racial and ethnic groups. For example, incidence of bladder cancer in men decreased overall and for every racial and ethnic group except American Indian and Alaska Native men, for which incidence increased significantly. Oral cavity and pharyngeal cancer also had discordant results. Overall and among White men, the incidence of cancers of the oral cavity and pharynx remained stable, but incidence of both cancers decreased significantly for Black and Hispanic men and increased significantly for Asian and Pacific Islander men and American Indian and Alaska Native men. Incidence of liver cancer was stable from 2014 to 2018 among men overall as well as for Black men and Hispanic men, but incidence increased for White and American Indian and Alaska Native men and decreased among Asian and Pacific Islander men. These results demonstrate the importance of disaggregated data when measuring incidence trends.

Among women, increases in the incidence of kidney and pancreatic cancer were observed across all racial and ethnic groups. Incidence of cancers of the lung and bronchus, bladder, and colon and rectum decreased among women for most racial and ethnic population groups, although some racial and ethnic population groups showed no significant change. However, the overall trend at times hid significant changes among some population groups. For example, incidence of cervical cancer was stable from 2014 to 2018 among women overall, as well as among White, American Indian and Alaska Native, and Hispanic women, but there were significant decreases in the incidence of cervical cancer among Black women and Asian and Pacific Islander women. Similarly, incidence of stomach cancer did not change overall or for White women and American Indian and Alaska Native women, but it decreased significantly among Black, Asian and Pacific Islander, and Hispanic women.

Finally, among women, the directionality of incidence for some cancers was discordant among the various racial and ethnic populations. For example, incidence of oral and pharyngeal cancer increased overall and for White women, but it decreased significantly for Black women. Incidence of liver cancer increased overall and for White, Hispanic, and American Indian and Alaska Native women, but decreased significantly for Asian and Pacific Islander women. These differences in cancer disparities by race and ethnicity are likely due to a combination of complex factors, including SES and cultural, social, and environmental factors, which may warrant further investigation (American Association for Cancer Research 2022).

Cancer Death Rates

As reported by Cronin and colleagues (2022), from 2001 to 2019, the decline in the overall rate of death from cancer among men averaged 1.8% per year from 2001 to 2015 and accelerated to 2.3% per year during 2015–2019. Among women, the decline in the rate of death from cancer averaged 1.4% per year during 2001–2016 and accelerated to 2.1% per year during 2016–2019. During 2015–2019, the overall death rate from cancer among men and women was 152.4 per 100,000 population; the rate was higher among men (181.4 per 100,000 population) than among women (131.1 per 100,000 population).

Lung and bronchus cancers were the leading cause of cancer deaths among men of all racial and ethnic population groups from 2015 to 2019. By race and ethnicity, the rate of death from lung and bronchus cancers was highest among Black men (54.0 per 100,000 population), followed by White men (47.0 per 100,000 population), American Indian and Alaska Native men (42.3 per 100,000 population), Asian and Pacific Islander men (26.9 per 100,000 population), and was lowest among Hispanic men (22.1 per 100,000 population).

Over the fixed 5-year interval from 2015 to 2019, the largest decline in the death rate from cancer was reported for lung and bronchus cancers among men (AAPC = −5.4%). Statistically significant declines in the death rate for lung and bronchus cancers were observed among men overall (AAPC = −5.0%) and among each racial and ethnic population group. The AAPC ranged from −4.9% among American Indian and Alaska Native men and Hispanic men to −6.1% among Asian and Pacific Islander men, though confidence intervals overlapped across groups.

Among women from 2015 to 2019, lung and bronchus cancers were the leading cause of cancer death for all racial and ethnic population groups with the exception of Hispanic women, for which lung cancer was the second most common cancer death (after breast cancer). From 2015 to 2019, the death rate of lung and bronchus cancers was highest among White (34.2 per 100,000 population), American Indian and Alaska Native (31.0 per 100,000 population) and Black women (29.2 per 100,000 population) and lowest for Asian and Pacific Islander (15.9 per 100,000 population) and Hispanic women (11.8 per 100,000 population). Over this fixed 5-year interval, the largest AAPC was observed for the decline in the death rate of lung and bronchus cancers among women (AAPC = −4.2%). By race and ethnicity, the steepest declines in the death rate of lung and bronchus cancers were observed among Hispanic women (AAPC = −4.7%) and Black women (AAPC = −4.4%); declines were less steep for White (AAPC = −3.9%), Asian and Pacific Islander (AAPC = −3.3%), and American Indian and Alaska Native (AAPC = −2.2%) women.

For other smoking-caused cancers, significant declines in the death rate from 2015 to 2019 were observed for urinary bladder cancer (men: AAPC = −1.5%; women: AAPC = −0.6%), cervical cancer (women: AAPC = −0.8%), esophageal cancer (men: AAPC = −1.2%; women: AAPC = −1.5%), kidney and renal pelvis cancers (men: AAPC = −2.6%; women: AAPC = −1.5%); colon and rectum cancers (men: AAPC = −2.1%; women: AAPC = −2.0%), laryngeal cancer (men, only: AAPC = −2.5%), and stomach cancer (men: AAPC = −2.5%; women: AAPC = −1.9%). A significant increase in the rate of death from pancreatic cancer (AAPC = 0.2% among both men and women) was observed during this period. Death rates for other smoking-caused cancers (liver cancer and cancers of the oral cavity and pharynx) were stable from 2015 to 2019.

For men, mortality trends across racial and ethnic populations were consistent with the overall trend for the decreases in lung and bronchus cancer and stomach cancer and mostly consistent with the overall decrease in mortality for esophageal, kidney, larynx and for colon and rectal cancer. However, for the increase in pancreatic cancer and the decrease in bladder cancer mortality, overall results were driven by the significant trends for White men with the other racial and ethnic populations demonstrating stable mortality rates from 2014 to 2018. Discordant trends were observed for liver cancer mortality. There was no change in liver cancer mortality observed overall or for White or Hispanic men, but significant decreases in mortality were reported for Black and for Asian and Pacific Islander men and a significant increase was seen for American Indian and Alaska Native men. Discordant trends were also reported for oral and pharyngeal cancer mortality. There was no change in oral and pharyngeal cancer mortality overall or among Asian and Pacific Islander or American Indian and Alaska Native men, but there was a significant increase in oral and pharyngeal cancer mortality for White men and a significant decrease in mortality for Black and Hispanic men, once again demonstrating the importance of disaggregated data.

For women, trends in mortality from 2014 to 2018 were consistent across racial and ethnic populations for the decreases in mortality for lung and bronchus, kidney, and stomach cancers. These trends were also mostly consistent across racial and ethnic populations for the decreases in mortality for cancers of the bladder, esophagus, and cervix and for colon and rectal cancer. For pancreatic cancer, despite an overall increase in mortality, significant decreases were reported for Black women and for Asian and Pacific Islander women; mortality rates were stable for White, Hispanic, and American Indian and Alaska Native women. Discordant results were also observed for liver cancer. There was no change in liver cancer mortality overall or for White, Black, or for American Indian and Alaska Native women, but a significant increase in liver cancer mortality among Hispanic women and a significant decrease in mortality among Asian and Pacific Islander women was observed. Oral cavity and pharyngeal cancer also had discordant mortality trends. The death rate was stable for oral cavity and pharyngeal cancer overall and among Hispanic women, but oral cavity and pharyngeal cancer mortality increased significantly among White women and decreased significantly among Black and Asian and Pacific Islander women. As previously described, discordant mortality trends by race and ethnicity are likely due to a combination of complex socioeconomic, cultural, social, and environmental factors (American Association for Cancer Research 2022).

Chronic Obstructive Pulmonary Disease

COPD includes a group of diseases causing restricted airflow and breathing issues; emphysema and chronic bronchitis are included in COPD (CDC n.d.b). The most common symptoms of COPD include coughing and wheezing; excess production of phlegm, mucus, or sputum; shortness of breath; and trouble breathing deeply (CDC n.d.b).

Cigarette smoking is a primary cause of COPD and the primary risk factor for the worsening of COPD (CDC 2012; USDHHS 2014). On the basis of data from the 2017 Behavioral Risk Factor Surveillance System (BRFSS), 6.2% (95% CI, 6.0–6.3) of U.S. adults indicated that they had been diagnosed with COPD by a healthcare provider (Wheaton et al. 2019). The prevalence of a diagnosis of COPD was higher among adults who currently smoke (15.2%; 95% CI, 14.7–15.7) and adults who formerly smoked (7.6%; 95% CI, 7.3–8.0) than among adults who never smoked (2.8%; 95% CI, 2.7–2.9) (Wheaton et al. 2019). Among all adults, the prevalence of a COPD diagnosis was higher among (a) women (6.8%; 95% CI, 6.6–7.0) than among men (5.5%; 95% CI, 5.4–5.7) and (b) older adults (≥65 years: 12.8%; 95% CI, 12.5–13.2) than among younger adults (55–64 years: 10.6%; 95% CI, 10.2–11.0; 45–54 years: 6.3%; 95% CI, 6.0–6.7; and 18–44 years: 2.7%; 95% CI, 2.5–2.8).

The prevalence of COPD also varies across racial and ethnic population groups. Using data from the 2017 BRFSS, Wheaton and colleagues (2019) found that the prevalence of COPD was significantly higher among American Indian and Alaska Native adults (11.9%; 95% CI, 10.3–13.7) than among non-Hispanic White (6.7%; 95% CI, 6.5–6.8), non-Hispanic Black (6.6%; 95% CI, 6.1–7.1), Hispanic (3.6%; 95% CI, 3.2–3.9), and Asian (1.7%; 95% CI, 1.2–2.5) adults. The prevalence of COPD was significantly lower among Hispanic adults than among White, Black, and American Indian and Alaska Native adults. The prevalence of COPD was significantly lower among Asian adults than it was among all other racial and ethnic population groups.

Using data from the 2017 BRFSS, Wheaton and colleagues (2019) also reported that the prevalence of COPD was higher among adults with other health conditions than adults without such conditions. For example, the prevalence of COPD was higher among adults with asthma (19.5%; 95% CI, 19.0–20.1) than it was among adults without asthma (4.1%; 95% CI, 4.0–4.2). Additionally, the prevalence of COPD increased with an increasing number of other chronic conditions (including coronary heart disease, stroke, diabetes, cancer, arthritis, kidney disease, and depressive disorder): no other chronic conditions (2.5%; 95% CI, 2.4–2.7), one chronic condition (5.8%; 95% CI, 5.5–6.1), two chronic conditions (12.6%; 95% CI, 11.9–13.4), three chronic conditions (20.2%; 95% CI, 18.1–22.5), and four or more chronic conditions (34.4%; 95% CI, 30.3–38.8). On the basis of data from the 2020 NHIS, as reported by the American Lung Association, the prevalence of a diagnosis of anxiety or depression is more than twice as high among people with COPD (43.5%) than it is among people without COPD (20.5%)1 (American Lung Association n.d.).

COPD is the primary cause of death from chronic lower respiratory diseases, which was the fourth leading cause of death in the United States in 2019 (Xu et al. 2021). Using the NCHS’s Underlying Causes of Death data compiled from the CDC Wonder Online database, the American Lung Association reported that the overall number of deaths from COPD in 2020 was higher among women (77,252) than among men (72,302); however, the age-adjusted rate of death from COPD was higher among men (39.2 per 100,000 men) than among women (36.3 per 100,000 women) (American Lung Association n.d.). Although COPD death rates have declined overall, declines have been limited to men in recent years (Zarrabian and Mirsaeidi 2021; Carlson et al. 2022; American Lung Association n.d.). For example, during 1999–2019, overall age-adjusted death rates for COPD did not change significantly among women but declined significantly among men by an average of 1.3% per year (AAPC = −1.3%) (Carlson et al. 2022). In general, rates of misdiagnosis or delayed diagnosis of COPD tend to be higher among women than among men, which may lead to more advanced disease at diagnosis and potentially less effective treatments in women (Carlson et al. 2022; CDC n.d.b). Other anatomical, hormonal, and behavioral differences by sex may influence differences in COPD morbidity and mortality between men and women (Aryal et al. 2014; CDC n.d.b).

By race and ethnicity, the highest rate of death from COPD in 2020 was observed among White adults (43.6 per 100,000 men and 37.9 per 100,000 women) followed by American Indian and Alaska Native adults (35.8 per 100,000 men and 26.5 per 100,000 women), Black adults (34.8 per 100,000 men and 22.5 per 100,000 women), Hispanic adults (18.7 per 100,000 men and 12.4 per 100,000 women), and Asian and Pacific Islander adults (13.8 per 100,000 men and 6.6 per 100,000 women) (American Lung Association n.d.). From 1999 to 2020, the absolute decline (i.e., the magnitude of difference) in the rate of death from COPD was similar among White (by 6.6 per 100,000 population; from 47.0 to 40.4 per 100,00 population), Black (by 6.2 per 100,000 population; from 29.9 to 23.7 per 100,000 population), and Hispanic (by 6.6 cases per 100,000 population; from 21.6 to 15.0 per 100,000 population) people (American Lung Association n.d.).

In 2019, death rates from COPD were higher in nonmetropolitan areas than in urban areas. From 1999 to 2019, urban–rural disparities in COPD death rates became more pronounced among both women and men (Carlson et al. 2022). The absolute disparity in the COPD death rate between large, central metropolitan areas (urban) and noncore areas (rural) increased by 34.5 deaths per 100,000 population among women and by 13.3 deaths per 100,000 population among men. Among women from 1999 to 2019, the rate of death from COPD increased significantly in 18 states, with the steepest increase observed in Arkansas (AAPC = 2.9%); death rates among women declined in 17 states, with the steepest decline observed in California (AAPC = −1.9%). Among men, the rate of death from COPD increased in one state (Arkansas, AAPC = 0.5%) and declined in 45 states, with the steepest decline observed in Alaska (AAPC = −4.2%) (Carlson et al. 2022).

Analyses of data from numerous reports suggest a clear association between socioeconomic gradients and COPD prevalence, mortality, severity, and quality of life (Hersh et al. 2011; CDC 2012; Jackson et al. 2013; Pleasants et al. 2013, 2015; Wheaton et al. 2015, 2016, 2019; Helms et al. 2017; Carlson et al. 2023; American Lung Association n.d.). For example, on the basis of 2017 BRFSS data, the prevalence of COPD was inversely associated with educational attainment; the prevalence of COPD was highest among people with less than a high school diploma (10.4%, 95% CI, 9.9–11.0) and lowest among people with a college degree or above (2.7%; 95% CI, 2.6–2.9) (Wheaton et al. 2019). Additionally, on the basis of 2020 NHIS data as reported by the American Lung Association (n.d.), the prevalence of COPD decreased with increasing family income (income-to-poverty ratio: <1 = 10.1%; 1–<2 = 7.5%; and ≥2 = 3.6%).

Using data from 16 states administering the Social Determinants of Health module on the 2017 BRFSS, Carlson and colleagues (2023) analyzed the relationship between self-reported COPD and measures of economic instability and stress. Findings suggest that adults with COPD were more likely to report financial instability (not having enough money or having just enough money at the end of the month; being unable to pay mortgage, rent, or utility bills; and inability to afford food or to eat well balanced meals) than adults without COPD. Similarly, adults with COPD were more likely to report experiencing stress (all or most of the time) than adults without COPD.

Cardiovascular Disease

Cardiovascular disease encompasses a range of clinical heart and circulatory conditions, including coronary heart disease, stroke, congestive heart failure, coronary artery disease, and peripheral arterial disease (USDHHS 2014; Tsao et al. 2023). The association between cigarette smoking and coronary heart disease was first established in the 1964 Surgeon General’s report (U.S. Department of Health, Education, and Welfare 1964). The evidence of a causal association between smoking and cardiovascular disease was further elucidated in subsequent Surgeon General’s reports, and a major conclusion of the 1983 report, The Health Consequences of Smoking: Cardiovascular Disease, was that “cigarette smoking is a major cause of coronary heart disease in the United States for both men and women. Because of the number of persons in the population who smoke and the increased risk that cigarette smoking represents, it should be considered the most important of the known modifiable risk factors for CHD” (USDHHS 1983, p. 6).

This section summarizes key findings from the annual Statistical Update from the American Heart Association, Heart Disease and Stroke Statistics–2023 Update: A Report from the American Heart Association (Tsao et al. 2023).

On the basis of NHANES data during 2017 to March 2020 (combined 2017–2018 cycle with the partial 2019–2020 cycle that was halted due to the COVID-19 pandemic), the prevalence of cardiovascular disease (including coronary heart disease, heart failure, and stroke) was 9.9%2 among adults 20 years of age and older, corresponding to an estimated 28.6 million adults (Tsao et al. 2023). Among men, the prevalence of cardiovascular disease was similar among non-Hispanic Black (11.3%) and non-Hispanic White (11.3%) men, followed by Hispanic men (8.7%) and non-Hispanic Asian men (6.9%). Among women, the prevalence of cardiovascular disease was highest among non-Hispanic Black women (11.1%), followed by non-Hispanic White (9.2%), Hispanic (8.4%), and non-Hispanic Asian (4.9%) women (Tsao et al. 2023).

The prevalence of cardiovascular disease and hypertension—a risk factor for the development of cardiovascular disease—was 48.6% among adults 20 years of age and older, corresponding to an estimated 127.9 million adults (Tsao et al. 2023). Among men, the prevalence of cardiovascular disease and hypertension was highest for non-Hispanic Black men (58.9%) and similar among Hispanic (51.9%), non-Hispanic Asian (51.5%), and non-Hispanic White (51.2%) men (Tsao et al. 2023). Among women, the prevalence of cardiovascular disease and hypertension was highest for non-Hispanic Black women (59.0%) followed by non-Hispanic White women (44.6%), non-Hispanic Asian women (38.5%), and Hispanic women (37.3%) (Tsao et al. 2023).

Using data from the 2011–2016 NHANES, Bundy and colleagues (2021) estimated that 12.8% of cardiovascular disease events (including incident nonfatal as well as fatal events) were attributable to smoking. By race and ethnicity, the proportion of cardiovascular disease events attributable to smoking was higher among Black adults (population-attributable fraction [PAF] = 17.2%) than among adults who were White, Mexican American, other Hispanic, and non-Hispanic Asian, as well as adults of other races (combined; PAF = 10.1%), although confidence intervals overlapped (Bundy et al. 2021). Using data from adults 20 years and older from the 1988 to 2016 NHANES, Han and colleagues (2019) estimated that the PAF of mortality from cardiovascular disease attributable to smoking was 10.7%.

For the United States overall during 2018–2020, the age-adjusted death rate for cardiovascular disease (defined using the International Classification of Diseases, 10th Revision codes [ICD 10] I00 to I99) was 218.8 per 100,000 population, which represented a 9.8% decline in the cardiovascular disease death rate from 2008 to 2010 (Tsao et al. 2023). By U.S. state and territory (including the District of Columbia and Puerto Rico), the age-adjusted death rate during 2018–2020 ranged from 146.7 per 100,000 population in Puerto Rico and 167.0 per 100,000 population in Minnesota to 307.4 per 100,000 population in Mississippi. The age-adjusted death rate for coronary heart disease (defined as ICD 10 codes I20 to I25) during 2018–2020 was 90.2 per 100,000 population overall, which was a 27.2% decline from 2008 to 2010. By state, the age-adjusted death rate for coronary heart disease ranged from 59.3 per 100,000 population in Minnesota to 131.0 per 100,000 population in Arkansas. The age-adjusted death rate of stroke (ICD 10 codes I60 to I69) during 2018–2020 was 37.6 per 100,000 population overall, which was a 10.8% decline from 2008 to 2010. The age adjusted death rate of stroke ranged from 23.7 per 100,000 population in Puerto Rico and 24.3 per 100,000 population in New York to 52.8 per 100,000 population in Mississippi.

Of all deaths attributable to cardiovascular disease in the United States in 2020, 41.2% were due to coronary heart disease, 17.3% to stroke, 12.9% to high blood pressure, 9.2% to heart failure, 2.6% to diseases of the artery, and 16.8% to other cardiovascular disease categories (Tsao et al. 2023). Cigarette smoking is causally associated with many of these diseases, including coronary heart disease and stroke, which account for the majority of cardiovascular disease deaths in the United States (USDHHS 1983, 2014). Although cigarette smoking can cause temporary increases in blood pressure (Rhee et al. 2007), evidence is evolving about the long-term impacts, including the possibly synergistic interactions, of cigarette smoking and high blood pressure on cardiovascular disease outcomes (USDHHS 1983, 2014). Additionally, using data from the Coronary Artery Risk Development in Young Adults study, Luehrs and colleagues (2021) found evidence of higher pulse pressure (difference between systolic blood pressure and diastolic blood pressure) among people who smoked compared with people who never smoked, which may confer, at least partially, a higher risk of cardiovascular disease among people who smoke.

Cardiovascular Health

According to the American Heart Association, the use of tobacco products (including combustible tobacco products and e-cigarettes) and exposure to secondhand tobacco smoke have adverse effects on overall cardiovascular health (Tsao et al. 2023).

Using the American Heart Association’s Life’s Simple 7—a composite score of heath metrics including smoking status, body mass index, physical activity, healthy diet, total cholesterol, blood pressure, and blood glucose—data from the 2011–2016 NHANES estimated that 70% of major cardiovascular disease events in the United States, including non-fatal myocardial infarction, stroke, heart failure, or death from cardiovascular disease, were attributable to having low (0–8 points [out of a possible 14 points]) or moderate (9–11 points) cardiovascular health scores (Bundy et al. 2021). Better overall cardiovascular health scores can attenuate the risk of mortality from cardiovascular diseases (Tsao et al. 2023). Bundy and colleagues (2021) estimate up to 2 million cardiovascular disease events could be prevented per year if people with low and moderate cardiovascular health scores could achieve high (12–14 points) cardiovascular health scores.

Life’s Simple 7 was updated and rescored in 2022 as Life’s Essential 8 (Lloyd-Jones et al. 2022). This composite metric assigns scores for specific health behaviors (nicotine exposure—including combustible tobacco and e-cigarette use; diet; physical activity; and sleep health) and health factors (body mass index, blood lipids, blood glucose, and blood pressure). The Life’s Essential 8 cardiovascular health scores can be measured or analyzed on a continuous scale (with scores ranging from 0 to 100) or categorized as low (scores of 0–49), moderate (scores of 50–79), or high (scores of 80–100) (Lloyd-Jones et al. 2022). By race and ethnicity, mean overall cardiovascular health scores—as measured by the Life’s Essential 8 using data from the 2013 to March 2020 NHANES—were significantly lower among non-Hispanic Black adults (59.7; 95% CI, 58.4–60.9) than among Hispanic (63.5; 95% CI, 62.2–64.8), non-Hispanic White (66.0; 95% CI, 64.8–67.2), and Non-Hispanic Asian (69.6; 95% CI, 68.1–71.1) adults (Tsao et al. 2023). Notably, cardiovascular health scores were significantly higher among Non-Hispanic Asian adults than among adults in other racial and ethnic groups.

As described earlier, better overall cardiovascular health scores can attenuate the risk of mortality from cardiovascular diseases (Tsao et al. 2023). Findings from multiple studies have reported this strong inverse and stepwise association between the number of cardiovascular health components at ideal levels and (a) all-cause mortality from cardiovascular disease and ischemic heart disease and (b) morbidity associated with cardiovascular disease, heart disease, and subclinical measures of atherosclerosis (Folsom et al. 2015; Shay et al. 2015; González et al. 2016; Ogunmoroti et al. 2017; Spahillari et al. 2017; Oyenuga et al. 2019; Tsao et al. 2023). Additionally, several studies have found disparities in achieving high cardiovascular health scores or in having worsening cardiovascular health scores over time. For example, less ideal cardiovascular health outcomes have been observed among adults with lower income and lower educational attainment (Caleyachetty et al. 2015; Jankovic et al. 2021; Johnson et al. 2022; Lassale et al. 2022), from minoritized population groups (specifically non-Hispanic Black adults) (Caleyachetty et al. 2015; Zheng et al. 2021; Lassale et al. 2022), among males (Jankovic et al. 2021), and by geographic region (specifically clustered in the southern United States among women of childbearing age) (Zheng et al. 2021). As discussed in Chapter 2, tobacco use is higher among many of these population groups.

Summary of the Evidence

This section described recent trends in incidence, prevalence, and mortality due to major smoking-caused diseases (i.e., cancer, COPD, and cardiovascular disease) by sociodemographic characteristics, including race and ethnicity, income level, educational attainment, and urbanicity, where available.

The incidence of smoking-related cancers of the pancreas, kidney and renal pelvis, liver, and oral cavity and pharynx increased among men and women from 2014 to 2018, and the trends for liver and for oral and pharyngeal cancers varied among racial and ethnic population groups (Cronin et al. 2022). Multiple factors likely contribute to the increasing incidence of some cancers, with smoking potentially interacting with some of these factors, such as alcohol consumption, to increase cancer risk (Boffetta and Hashibe 2006; Scoccianti et al. 2013; Connor 2017). For example, increasing incidence trends of cancers of the oral cavity and pharynx are limited to subsites that are strongly associated with human papillomavirus infection (Chaturvedi et al. 2011; Ellington et al. 2020; Islami et al. 2021). Additionally, the incidence of cancers associated with overweight and obesity, including kidney and liver cancers, are increasing (Lauby-Secretan et al. 2016; Islami et al. 2021; Cronin et al. 2022). Furthermore, increasing incidence of liver cancer has been attributed to a high prevalence of hepatitis C virus infection in the birth cohort born between 1945 and 1965 (Ryerson et al. 2016; Hofmeister et al. 2019).

The decreasing incidence of many smoking-caused cancers—including lung and bronchus cancers—primarily reflects declines in the prevalence of smoking and other risk factors, as well as improvements in cancer screening behaviors and diagnostic practices that have contributed to improved detection of disease and improvements in treatment (Howlader et al. 2020; Cronin et al. 2022; Shiels et al. 2023). For example, use of lung cancer screening in the United States increased slightly between 2015 (3.9%) and 2020 (6.5%) (Jemal and Fedewa 2017; Cronin et al. 2022; Fedewa et al. 2022), which may have contributed to increases in the proportion of cases of lung cancer diagnosed at localized stages beginning around 2013 (Siegel et al. 2022). Additionally, the reduction in overall cancer mortality during 2015–2019 has been driven largely by steep declines in lung cancer death rates among men and women (Cronin et al. 2022). Despite this progress, lung cancer remains the leading cause of cancer death among men and women in the United States (Cronin et al. 2022; Siegel et al. 2022). As such, interventions, including tobacco use prevention, increased smoking cessation, increased use of cancer screening, and increased access to more effective treatments are important to further reduce the incidence and mortality of tobacco-related cancers. Furthermore, opportunities to reduce disparities in access and use of screening and more effective treatments are warranted (Shiels et al. 2023).

Although this chapter does not examine these factors in detail, cancer disparities exist across multiple measures—including survival, screening rates, and stage at diagnosis (NCI 2022). Together with additional social and structural barriers, bias from healthcare providers, whether conscious or unconscious, or mistrust of the healthcare system can influence whether people who smoke from different population groups seek care, get screened, or get treatment for tobacco cessation (NCI 2022). Because multiple, often compounding factors influence disparities in cancer incidence and mortality, addressing them requires comprehensive efforts to prevent and reduce commercial tobacco use and systemic, racial and ethnic, and institutional inequities (NCI 2017a, 2022a).

Cigarette smoking is a primary cause of COPD and the primary risk factor for the worsening of COPD (CDC 2012; USDHHS 2014). The overall prevalence of COPD is highest among American Indian and Alaska Native adults and is lowest among Asian adults (Wheaton et al. 2019), which is consistent with patterns in tobacco product use by race and ethnicity (see Chapter 2). Data also indicate a clear socioeconomic gradient associated with COPD, whereby the prevalence of and mortality from COPD is higher among people with lower income levels and lower educational attainment than among their respective counterparts (Wheaton et al. 2019; American Lung Association n.d.). Additionally, the prevalence of COPD is higher among people with other comorbidities (Wheaton et al. 2019; American Lung Association n.d.). Evidence also suggests that rates of COPD are higher among people who live in rural areas than among those who live in urban areas, and that, over time, the disparity in COPD mortality increased between urban and rural areas, particularly among women (Carlson et al. 2022).

About 1 in 10 U.S. adults (9.9%) have cardiovascular disease, including coronary heart disease, heart failure, and stroke, while nearly half of U.S. adults (48.6%) have cardiovascular disease and hypertension (a risk factor for cardiovascular disease) (Tsao et al. 2023). By race and ethnicity, the prevalence of cardiovascular disease and hypertension is highest among non-Hispanic Black women (59.0%) and men (58.9%) and lowest among Hispanic women (37.3%) (Tsao et al. 2023). Tobacco product use and exposure to secondhand tobacco smoke have adverse effects on overall cardiovascular health. Mean overall cardiovascular health scores are lower (i.e., worse) among non-Hispanic Black adults compared with adults from other racial and ethnic population groups and highest (i.e., better) among Non-Hispanic Asian adults. Additionally, disparities in attaining high cardiovascular health scores or in having worsening scores over time have been observed among non-Hispanic Black adults compared to non-Hispanic White adults, as well as by educational attainment, income level, and geographic region. These findings underscore the need to identify barriers to achieving high cardiovascular health across different population groups (Tsao et al. 2023).

When conducting research involving race and ethnicity, reporting separately the data for as many groups as possible helps to elucidate similarities and differences in the incidence and mortality of smoking-caused diseases. Further, efforts are warranted to explore health outcomes and the intersection of race and ethnicity and additional sociodemographic characteristics such as socioeconomic status. In 1997, the Office of Management and Budget required that the category for “Asian and Pacific Islander” people be reported separately as “Asian” people and as “Native Hawaiian or Other Pacific Islander” people (Federal Register 1997; Office of Minority Health 2021). Information presented in this section is not available for disaggregation within racial and ethnic population groups, but recent evidence from 2018 to 2020 suggests that large disparities in cancer mortality rates exist between the aggregate categories of Asian and Native Hawaiian or Other Pacific Islander people (Haque et al. 2023). Within each of these major categories of racial groups, data show that the prevalence of smoking varies (see Chapter 2). Therefore, the interpretation of the data for racial and ethnic population groups presented in this section must be approached with caution because aggregation may mask disparities within these populations.

Examining overall trends in the incidence and mortality of smoking-caused outcomes provides valuable data to inform progress and challenges related to eliminating smoking-caused morbidity. Disparities in incidence, prevalence, and mortality of smoking-caused cancers, COPD, and cardiovascular disease reflect multiple intersecting factors, including risk factors other than smoking—such as alcohol use, dietary intake, physical inactivity, or exposure to bacterial and viral infections (Singh and Jemal 2017; Goding Sauer et al. 2019; American Association for Cancer Research 2022; Cronin et al. 2022; NCI 2022; Tsao et al. 2023)—social determinants of health (i.e., the conditions where people are born, live, learn, work, play, worship, and age that affect health, functioning, and quality of life), behavior, biology, and genetics (American Association for Cancer Research 2022; Cronin et al. 2022; NCI 2022; Tsao et al. 2023; Office of Disease Prevention and Health Promotion n.d.). Examining these data for specific population groups can also provide insight into groups to prioritize for future interventions and resource allocation.

Smoking-Attributable Mortality Across U.S. Populations

CDC has produced estimates of the health and economic burdens attributable to cigarette smoking for almost 30 years through the Smoking-Attributable Mortality, Morbidity, and Economic Costs (SAMMEC) system. Epidemiologists, policymakers, public health practitioners, and other professionals have used these estimates to inform and support programs and policy initiatives that are intended to reduce smoking in the United States. The common approach for calculating PAF is as follows:

PAF=P(RR1)P(RR1)+1
where P is the prevalence of exposure and RR is the relative risk for mortality associated with that exposure. CDC’s calculation for smoking-attributable fraction (SAF) adapts the PAF as follows:
SAF=Pcs(RRcs1)+Pfs(RRfs1)Pcs(RRcs1)+Pfs(RRfs1)+1
such that Pcs and Pfs represent the prevalence of current and former smoking, respectively, at the population level and RRcs and RRfs represent the RR of mortality associated with current and former smoking, respectively, relative to people who never smoked.

Chapter 12 of the 2014 Surgeon General’s report offers additional details about the SAMMEC methodology, including its assumptions and limitations, and how SAFs are influenced by underlying RRs (USDHHS 2014). The health burden component of SAMMEC is based on the approach of Levin (1953), which involves the computation of PAFs (known as SAFs in SAMMEC) for diseases determined by the U.S. Surgeon General to have a causal relationship with cigarette smoking (Levin 1953; USDHHS 2004, 2014). In this chapter, estimates of the number of deaths attributable to smoking are calculated by multiplying the corresponding SAF for each population group by the total number of deaths in that population group.

As of 2014, cigarette smoking was causally associated with 27 diseases or adverse outcomes (Table 6.1). Five of these chronic diseases—lung cancer, coronary heart disease, other heart disease, cerebrovascular disease, and COPD—account for an estimated 80% of smoking-attributable mortality in the United States (USDHHS 2014). According to the 2014 Surgeon General’s report, cigarette smoking is causally linked to 12 cancers (USDHHS 2014). A range of estimates exists for the PAF of smoking for all cancer deaths, which represent calculations of specific population groups, prevalence estimates, and RR estimates for a given time period (USDHHS 2014). Additionally, analyses suggest that the PAF of cancer deaths attributable to smoking has declined over time due to the decline in the prevalence of smoking. For example, an analysis of the PAF for cancer deaths attributable to cigarette smoking in 2011 estimated PAFs of 51.5% for men and 44.5% for women (Siegel et al. 2015). More recently, Islami and colleagues (2022) estimated that, of the 418,563 total cancer deaths in 2019 among adults 25–79 years of age, 122,951 were attributable to smoking, for an overall PAF of 29.4% (men: 74,508 deaths, PAF = 33.1%; women: 48,536 deaths, PAF = 25.0%). By state, the estimated proportion of cancer deaths attributable to smoking in 2019 was lowest in Utah (PAF = 16.5%) and highest in Kentucky (PAF = 37.8%), which corresponds to states with lower and higher prevalence of smoking (see Chapter 2).

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Table 6.1

Diseases that are causally associated with or worsened by cigarette smoking.

Historically, national and state-based estimates of smoking-attributable mortality have been generated and reported by sex. However, reports on smoking-attributable mortality that are stratified by other factors relevant to health and smoking-related disparities, such as race and ethnicity, level of educational attainment, urbanicity, and geographic region (e.g., U.S. Census Region) are lacking, representing an important knowledge gap.

One reason for the absence of such estimates has been the general lack of group-specific RR estimates for smoking-attributable diseases, which are needed to estimate smoking-attributable mortality. Such data are often lacking because many population groups are underrepresented in large cohort studies of people who smoke and do not smoke. For example, some ethnic populations with lower SES are underrepresented in the Cancer Prevention Study II (Calle et al. 2002; USDHHS 2004), which is a well-known cohort study of 1.2 million American men and women volunteers that serves as a common source of data for RR estimates in analyses of SAFs (Calle et al. 2002; USDHHS 2004). Although analyses using estimates of smoking-attributable mortality based on Cancer Prevention Study II and other cohorts are considered scientifically sound for the overall U.S. population (Malarcher et al. 2000; USDHHS 2004, 2014), contemporary cohorts that are more representative of the current U.S. population are needed to produce appropriate population group estimates of smoking-attributable mortality.

The National Health Interview Survey and Linked Mortality Files

The National Center for Health Statistics (NCHS) links records from participants in large national surveys, such as the NHIS and the NHANES, which are designed to be representative of the civilian, noninstitutionalized U.S. population, to mortality information in the NDI. Information from these data sources enables researchers to conduct longitudinal analyses that describe health outcomes in relation to the baseline characteristics measured in these surveys.

RRs for mortality were computed using the NHIS Linked Mortality File (LMF) by current and former smoking status. To protect the privacy of decedents, work was conducted in the NCHS Research Data Center (CDC 2020). Specifically, this analysis used NHIS respondents who were surveyed during 1999 to 2014 with linked mortality data beginning in 2000 through December 31, 2015. All participants with sufficient identifying data were eligible for mortality linkage. Each survey record was screened to determine if it contained at least one of the following combinations of identifying data elements:

  1. Social Security number (SSN) (nine digits [SSN9] or last four digits [SSN4]), last name, first name
  2. SSN (SSN9 or SSN4), sex, month of birth, day of birth, year of birth
  3. Last name, first name, month of birth, year of birth

Any survey participant records that did not meet these minimum data requirements were ineligible for record linkage. On average, an estimated 94.8% of NHIS participants for the years 1999 to 2014 were eligible for mortality follow-up (NCHS 2019). Mortality for eligible survey respondents was primarily determined by matching identifying data between survey records to the NDI and supplemented with information from NHIS linkages with other sources, such as the Social Security Administration and Centers for Medicare & Medicaid Services. If a match was found for the NHIS respondent in the NDI, the respondent was assumed to be dead; if no match was found, the participant was assumed to be alive as of December 31, 2015.

The respondent’s smoking status was collected only at the time of their NHIS interview and not at mortality follow-up. To minimize bias in RR estimates attributable to potential changes in smoking status over time (e.g., initiation, relapse, or quitting), follow-up was restricted to 10 years, and participant data were censored thereafter. The demographic characteristics of the NHIS-NDI cohort by race (for non-Hispanic people or people of Hispanic origin) are shown in Table 6.2.

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Table 6.2

Demographic characteristics of participants by race and ethnicity, NHIS Linked Mortality File, 1999–2014.

Cause of Death

The NHIS-NDI LMF reports respondents’ specific underlying cause of death, which was coded using ICD-10 (Table 6.1). Initially, lung cancer, coronary heart disease, other heart disease, cerebrovascular disease, and COPD were examined as causes of death, as were grouped conditions that included all smoking-attributable diseases, all cancers, and all deaths. However, preliminary analyses of individual causes of death for sociodemographic groups resulted in small sample sizes, introducing sizeable error into the resulting estimates. Therefore, the following analyses focus on mortality from all causes combined (hereafter referred to as “all-cause mortality”).

Demographic Variables

All demographic variables—including smoking status—among respondents in the NHIS-NDI LMF cohort were determined based on respondents’ answers at the time of their NHIS interview. Baseline demographic characteristics and smoking status were assumed to be consistent during follow-up.

Age

Following standard SAMMEC methodology for estimating smoking-attributable mortality for adults (Levin 1953; USDHHS 2004, 2014), participants younger than 35 years of age at the time of their NHIS interview were excluded from analysis. Participants were categorized into four age strata: 35–54 years of age, 55–64 years of age, 65–74 years of age, and 75 years of age and older.

Race and Ethnicity

The analysis used NHIS-NDI data from 1999 to 2015 among non-Hispanic White, non-Hispanic Black, and Hispanic people only. Although other racial and ethnic groups were and remain of interest (e.g., American Indian and Alaska Native people, Asian American, Native Hawaiian, and Other Pacific Islander people), the small numbers of deaths for these population groups in the NHIS-NDI LMF precluded further analysis. Respondents indicated Hispanic ethnicity by responding affirmatively to the question “Do you consider yourself to be Hispanic or Latino?” They then were asked “What race or races do consider yourself to be? Please select one or more of these categories.”

For the analyses related to smoking-attributable mortality, the term Hispanic refers to people from any race who identify as Hispanic. American Indian and Alaska Native, Asian American, Black, Hispanic, Native Hawaiian, Other Pacific Islander, and White populations exclude those who identify as Hispanic. Although the risk of death for Hispanic ethnicity is not the same across all racial groups, due to sample sizes, race-Hispanic and race-non-Hispanic ethnicity could not be analyzed separately.

Level of Educational Attainment

Level of educational attainment at the time of respondents’ NHIS interview was based on responses to the question “What is the highest level of school you have completed or the highest degree you have received?” The survey included five mutually exclusive categories: (1) 8th grade or lower; (2) 9th–12th grade, no diploma; (3) high school diploma or GED (General Educational Development certificate); (4) some college, no degree; and (5) college degree or above.

Geographic Region

The analysis examined four census geographic regions based on the respondents’ state of residence at the time of the NHIS interview.

  • Northeast: Connecticut, Maine, Massachusetts, New Hampshire, Rhode Island, Vermont, New Jersey, New York, and Pennsylvania;
  • Midwest: Indiana, Illinois, Michigan, Ohio, Wisconsin, Iowa, Kansas, Minnesota, Missouri, Nebraska, North Dakota, and South Dakota;
  • South: Delaware, District of Columbia, Florida, Georgia, Maryland, North Carolina, South Carolina, Virginia, West Virginia, Alabama, Kentucky, Mississippi, Tennessee, Arkansas, Louisiana, Oklahoma, and Texas; and
  • West: Arizona, Colorado, Idaho, New Mexico, Montana, Utah, Nevada, Wyoming, Alaska, California, Hawai‘i, Oregon, and Washington state.

Urbanicity

The Office of Management and Budget determines metropolitan statistical areas using census data. Over time, however, the categorization of counties may change as fewer urban areas become essentially metropolitan areas because of population changes. The NCHS urbanization schemes are updated regularly to reflect changes to settlement patterns (Ingram and Franco 2014).

For the current analysis, among NHIS-NDI LMF participants, urbanicity at the time of the NHIS interview was determined by the 2013 NCHS Urban-Rural Classification Scheme for counties (Ingram and Franco 2014). These data are available only through the NCHS Research Data Center to protect the privacy of decedents (CDC 2019). Briefly, all counties in the United States were assigned to one of the six urbanization levels (large central metro, large fringe metro, medium metro, small metro, micropolitan, and noncore) ranging from the most urban to the most rural on the basis of the 2010 Office of Management and Budget metropolitan-nonmetropolitan classification of counties. Metropolitan counties (e.g., urban) included large central metro, large fringe metro, medium metro, and small metro counties; nonmetropolitan counties (e.g., rural) included micropolitan, and noncore communities.

Smoking Status

Respondents in the NHIS-NDI LMF were categorized as people who currently smoked, people who smoked in the past, or people who never smoked based on their responses at the time of their NHIS interview. People who currently smoked were defined as those who reported having smoked 100 or more cigarettes in their lifetime and who smoked every day or on some days at the time of the interview. People who smoked in the past were defined as those who reported having smoked at least 100 cigarettes during their lifetime but were not smoking at the time of the interview. People who never smoked were defined as those who had never smoked, or who had reported having smoked less than 100 cigarettes in their lifetimes (NCHS n.d.).

Trends and disparities in the prevalence of smoking by race and ethnicity, level of educational attainment, geographic region, and urbanicity are described in Chapter 2.

Estimates of Relative Risk of Mortality for Selected Sociodemographic Groups

Weighted NHIS-NDI LMF data were used to estimate the RR of mortality by group. The original NHIS adult sample weights were adjusted to account for respondents who were ineligible for linkage to the mortality follow-up (through December 31, 2015). Following standard procedures, the adjusted adult sample weights were divided by 17 (equal to the number of NHIS survey years) to compute the final analytic weights per person; more details about the NHIS-NDI LMF methodology can be found elsewhere (NCHS 2019).

The RRs for smoking-attributable diseases were computed for people who currently smoked and people who smoked in the past; the referent group was people who never smoked. For all sociodemographic groups considered, computed RRs were stratified by gender3 and age group. Deaths were assumed to be Poisson-distributed and conditional on number of years of follow-up. A multivariable Poisson regression model was built to compute RRs by smoking status for each age group and racial ethnic group. RRs were computed with a 95% CI; CIs were based on a normal approximation for the natural log RRs. RR estimates for American Indian and Alaska Native and Asian American, Native Hawaiian, and Other Pacific Islander people are omitted from this section because of insufficient numbers of deaths in each age group during the period of analysis.

Relative Risks of All-Cause Mortality

Race and Ethnicity

Table 6.3 presents estimated RRs of all-cause mortality by gender, race and ethnicity, and age group. For Hispanic, non-Hispanic White, and non-Hispanic Black men, and non-Hispanic White women who currently smoked (at the time of their interview), compared with people who never smoked, the RR of all-cause mortality increased from the 35- to 54-year-old age group to the 55- to 64-year-old age group before declining for the oldest age groups (65–74 years of age and 75 years of age and older). For non-Hispanic Black and Hispanic women who currently smoked compared with women who never smoked, the RR of all-cause mortality increased from the 35- to 54-year-old age group to the 65- to 74-year-old age group before declining among women 75 years of age and older. In general, these estimates were largest for non-Hispanic White people, followed by non-Hispanic Black adults, and lowest for Hispanic adults. This was true across all age groups and among men and women.

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Table 6.3

Estimated relative risks for all-cause mortality among people, 35 years of age and older, who currently smoked and who formerly smoked, by gender, race and ethnicity, and age; NHIS Linked Mortality File, 1999–2014.

Non-Hispanic White men and women who currently smoked and were 35–64 years of age had the highest RR estimates for all-cause mortality, with more than three times the mortality risk of people who never smoked. For Hispanic men and women 75 years of age and older, current smoking was not associated with a statistically significantly elevated RR of mortality compared with never smoking, although these results may have been the product of small numbers of observed deaths in those categories. White women who were younger than 65 years of age and currently smoked had an estimated risk of death that was three times that of their never-smoking counterparts. Black women who were younger than 75 years of age and who currently smoked had more than twice the risk of death compared with Black women in that age group who never smoked. Estimates of RR were generally highest in the 55- to 64-year-old age group across the three racial and ethnic groups for men and for non-Hispanic White women. For Black and Hispanic women, estimates of RR were highest in the 65- to 74-year-old age group.

For most population groups, people who smoked in the past (at the time of interview) had a moderately increased risk of mortality by gender, age group, and race or Hispanic origin compared with people who never smoked (RR <2.0). Specific groups of people who smoked in the past had RR estimates that were not statistically significantly different from that of people who never smoked, as indicated by the CIs crossing 1.0: non-Hispanic Black men (75 years of age and older: RR = 1.08), Hispanic women (35–64 years of age: RR = 0.81; 55–64 years of age: RR = 1.24; 75 years of age and older: RR = 1.14), and non-Hispanic Black women (35–54 years of age: RR = 1.23; 75 years of age and older: RR = 1.12). These non-significant findings may reflect declining RRs with increasing time since quit smoking (USDHHS 2020) or may be due to small sample sizes resulting in wider CIs.

Level of Educational Attainment

Table 6.4 presents RR estimates of all-cause mortality for men and women who, at the time of interview, currently smoked and people who smoked in the past by level of educational attainment and age group compared with people of the same level of educational attainment and age who never smoked. Across all age groups, genders, and levels of educational attainment, people who currently smoked had a significantly higher RR of all-cause mortality compared with their never-smoking counterparts. Currently smoking, college-educated men 65–74 years of age and currently smoking college-educated women 55–64 years of age at the time of interview had the highest RR (3.39 and 3.43, respectively) for mortality compared with their never-smoking counterparts.

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Table 6.4

Estimated relative risks for all-cause mortality among people, 35 years of age and older, who currently smoked and who formerly smoked, by gender, level of educational attainment, and age group, NHIS Linked Mortality File, 1999–2014.

With some exceptions, the magnitude of the RR was generally lower among people with an eighth-grade education or less who currently smoked at the time of interview (compared to their never-smoking counterparts) than were RRs among people with other levels of educational attainment. Furthermore, with some exceptions, RR estimates were generally higher among people with more than an eighth-grade education but less than a college degree who smoked (compared to their never-smoking counterparts) than they were among people with other educational attainment levels. Among men and women 75 years of age and older in all levels of educational attainment, RR estimates were similar and overlapping, ranging from 1.29 to 1.67.

Mortality RRs among people who smoked in the past (at the time of interview) were much lower than those among people who currently smoked (RRs among people who smoked in the past were ≤1.7); CIs overlapped for most estimates, leading to few differences by level of educational attainment, age group, and sex. Adults 35–54 years of age and 75 years of age and older who smoked in the past had lower mortality RR estimates (compared to people who never smoked) than the RR estimates among those 55–74 years of age. Compared to their never-smoking counterparts, mortality RR estimates for people with specific levels of educational attainment who smoked in the past did not differ significantly for men and women 35–54 years of age with less than an eighth-grade education; women 35–54 years of age with 9th- to 12th-grade education but no diploma; women 35–54 years of age with a high school degree or GED; and men 75 years of age and older with some college education but no degree. As stated previously, these non-significant findings may be due to small sample sizes.

Geographic Region

Across all geographic regions, people 75 years of age and older who currently smoked at the time of their NHIS interview had the lowest RR for mortality compared with their counterparts never smoked (Table 6.5), which may be due to competing causes of mortality and temporal trends in smoking by birth cohort. For example, because older birth cohorts started smoking at earlier ages and had higher smoking prevalence than younger cohorts, more members of older birth cohorts may have died from smoking-attributable causes before reaching age 75 (USDHHS 2014). People 55–64 years of age who currently smoked had the highest RR for mortality, on average, led by men in the Northeast (RR = 3.30) and women in the Midwest (RR = 3.38), which were more than three times the RR for mortality compared with people who never smoked in their respective regions and age groups. RR estimates for people who smoked in the past were highest in the Midwest for men and women 35–74 years of age in the Midwest; men and women 65–74 years of age who smoked in the past had more than 1.7 times the risk for mortality compared with their never-smoking counterparts.

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Table 6.5

Estimated relative risks for all-cause mortality among people, 35 years of age and older, who currently smoked and who formerly smoked, by gender, geographic region, and age group; NHIS Linked Mortality File, 1999–2014.

Urbanicity

Table 6.6 presents RR estimates for people who currently smoked and people who smoked in the past by urbanicity (at the time of their NHIS interview) compared to their never-smoking counterparts. In rural areas, women who currently smoked at the time of interview and were 35–54 years of age had higher RRs for mortality compared with women in the same age group who currently smoked in urban areas. There were no major differences in RR for mortality between people living in urban and rural places for other age and gender groups. Estimates followed similar patterns of highest RRs for men and women 55–65 years of age and lowest RRs for men and women 75 years of age and older. With respect to former smoking, the RR for mortality was highest (1.64) among women 55–64 years of age who lived in rural areas, although the magnitude of the RR for mortality was similar among other population groups studied based on overlapping CIs. The RR for mortality among women 35–54 years of age who smoked in the past and lived in either rural or urban areas was not statistically significant.

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Table 6.6

Estimated relative risks for all-cause mortality among people, 35 years of age and older, who currently smoked and who formerly smoked, by gender, urbanicity, and age group; NHIS Linked Mortality File, 1999–2014.

Smoking-Attributable Fractions in the United States, 2010–2018

To facilitate calculations of the SAF, the population-level prevalence estimates of current, former, and never smoking—pooled across the public use 2010–2018 NHIS data files—were stratified by age group, gender, race and ethnicity, educational attainment, and geographic region (Appendix Tables 6A.16A.3). Weights were pooled across years by dividing annual weights by 9 (equal to the number of NHIS survey years) following standard procedures. Pooled prevalence estimates by urbanicity were not obtained because of the absence of this information in 2010–2018 NHIS public-use files.

Race and Ethnicity

Among men, an estimated 9–22% of all deaths of Hispanic, 12–39% of non-Hispanic White, and 7–39% of non-Hispanic Black men were attributed to smoking; the range varied by age group (Table 6.7). Among women, smoking was attributed to 1–13% of all deaths of Hispanic, 10–38% of non-Hispanic White, and 7–22% of non-Hispanic Black women. Among men, SAFs were highest among non-Hispanic White men who were 35–64 years of age (38–39%) and among non-Hispanic Black men who were 55–64 years of age (39%). Among women, SAFs were highest among non-Hispanic White women who were 35–64 years of age (35–38%) and lowest among Hispanic women who were 35–54 years of age and 75 years of age and older (<5%). For non-Hispanic Black and White people, SAFs peaked at 55–64 years of age before declining at older ages. For Hispanic people, SAFs peaked at 65–74 years of age.

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Table 6.7

Smoking-attributable fractions for all-cause mortality by gender, age group, and race and ethnicity; NHIS Linked Mortality File, 1999–2014.

Level of Educational Attainment

Table 6.8 shows SAFs by level of educational attainment. Among men, 12–16% of all deaths for those with an 8th-grade education or less were attributed to smoking, 15–44% for those with a 9th- to 12th-grade education but no diploma, 13–35% for those with a high school diploma or GED, 8–37% for those with some college education but no degree, and 9–17% for those with a college degree or above. Among women, 6–19% of all deaths for those with an 8th-grade education or less were attributed to smoking, 14–40% for those with a 9th- to 12th-grade education but no diploma, 12–33% for those with a high school diploma or GED, 12–30% for those with some college education but no degree, and 6–21% for those with a college degree or above. SAFs peaked at 55–64 years of age among men and women with more than an 8th-grade education but less than a college degree and among women with college degrees. In contrast, SAFs peaked at 65–74 years of age among men and women with an 8th-grade education or less and among men with a college degree or higher.

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Table 6.8

Smoking-attributable fractions for all-cause mortality by gender, age group, and level of educational attainment; NHIS Linked Mortality File, 1999–2014.

Geographic Region

Table 6.9 shows SAFs by geographic region. Among men, 12–34% of all deaths in the Northeast, 14–39% in the Midwest, 10–36% in the South, and 14–31% in the West were attributable to smoking. Among women, 12–27% of all deaths in the Northeast, 7–37% in the Midwest, 9–30% in the South, and 9–22% in the West were attributable to smoking.

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Table 6.9

Smoking-attributable fractions for all-cause mortality by gender, age, and geographic region; NHIS Linked Mortality File, 1999–2014.

Urbanicity

SAFs could not be calculated by urbanicity because the prevalence of smoking stratified by the intersection of urbanicity, gender, and age group was not available in the 2010–2018 NHIS public use data file.

Smoking-Attributable Mortality in the United States by Race and Ethnicity, 2010–2018

Tables 6.10 and 6.11 present the estimated number of deaths from all causes attributable to smoking among non-Hispanic Black, non-Hispanic White, and Hispanic adults who smoked and formerly smoked from 2010 to 2018 by gender, age group, and race and ethnicity. Estimates are presented after being rounded to the nearest 100 people.

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Table 6.10

Total deaths, smoking-attributable mortality, and average annual smoking-attributable mortality per 100,000 population for all causes of death among people who currently smoked and who formerly smoked, by gender and age group; 2010–2018; United (more...)

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Table 6.11

Total deaths, smoking-attributable mortality, and average annual smoking-attributable mortality per 100,000 population for all causes of death among people who currently smoked and who formerly smoked, by gender and race and ethnicity; 2010–2018; (more...)

To calculate the estimated total number of smoking-attributable deaths, SAFs were applied to the total number of deaths during 2010–2018 for selected populations from the National Vital Statistics System mortality data extracted from CDC Wonder among adults 35 years of age and older (CDC n.d.a). The average annual smoking-attributable mortality was calculated as the total number of smoking-attributable deaths divided by the number of years (n = 9) included in the analysis. The average annual smoking-attributable mortality rate (per 100,000 population) was calculated as the total number of smoking-attributable deaths divided by the total population size for selected population groups 35 years of age and older from the U.S. Census Bureau single-race population estimates extracted from CDC Wonder (CDC n.d.c).

Data for deaths are from the Multiple Cause of Death Files for 1999–2019, as compiled from data provided by the 57 vital statistics jurisdictions through the Vital Statistics Cooperative Program (CDC n.d.a). National mortality and population data by race and Hispanic origin, age group, and gender were obtained from CDC Wonder. Death counts were restricted to select populations with non-missing data. For this analysis, deaths among American Indian and Alaska Native people, Asian American and Pacific Islander people, and people with unknown ethnicity were excluded because of small sample sizes that limit estimates of RR. Due to data issues that would complicate presentation of results, analyses of smoking-attributable deaths by urbanicity, geographic region, and level of educational attainment were not conducted.

From 2010 to 2018, at least 4,259,400 smoking-attributable deaths were estimated to have occurred. On average each year, at least 473,300 smoking-attributable deaths were estimated to have occurred (277,100 deaths among men and 196,200 among women) among non-Hispanic White, non-Hispanic Black, and Hispanic adults (Table 6.10). The average annual smoking-attributable death rate among non-Hispanic White, non-Hispanic Black, and Hispanic adults from 2010 to 2018 was an estimated 289.9 deaths per 100,000 population (365.9 deaths per 100,000 men and 237.5 deaths per 100,000 women). The estimated number of annual smoking-attributable deaths increased by age group for women, but for men, the estimated number peaked at 65–74 years of age before declining among those 75 years of age and older. However, the smoking-attributable death rate was highest among men and women 75 years of age and older: 914.5 deaths per 100,000 men and 680.5 deaths per 100,000 women.

Table 6.11 shows the estimated number of smoking-attributable deaths among Hispanic, non-Hispanic Black, and non-Hispanic White men and women. On average, an estimated 15,100 smoking-attributable deaths occurred each year among Hispanic adults (11,400 deaths among men and 3,800 deaths among women), 50,600 among non-Hispanic Black adults (31,700 deaths among men and 19,000 deaths among women), and 407,500 among non-Hispanic White adults (234,100 deaths among men and 173,500 deaths among women). Of all deaths that occurred among Hispanic men and women, 10% were attributed to smoking. In addition, 18% of all deaths for non-Hispanic Black men and women and 20% of all deaths for non-Hispanic White men and women were attributed to smoking.

The average annual smoking-attributable death rate from 2010 to 2018 was approximately 69.2 deaths per 100,000 Hispanic people (106.0 deaths per 100,000 Hispanic men and 33.7 deaths per 100,000 Hispanic women), 266.9 deaths per 100,000 Black people (369.1 deaths per 100,000 Black men and 182.5 deaths per 100,000 Black women), and 346.7 deaths per 100,000 White people (414.7 deaths per 100,000 White men and 283.9 deaths per 100,000 White women). From 2010 to 2018, men accounted for 75% of all smoking-attributable deaths in the Hispanic population, 63% of such deaths in the non-Hispanic Black population, and 57% of such deaths in the non-Hispanic White population.

The NHIS-NDI-LMF did not include sufficient data on American Indian and Alaska Native people and Asian American and Pacific Islander people to allow for longitudinal analysis of these population groups. Therefore, conclusions about mortality rates attributable to smoking for these populations cannot be made using these data. However, evidence from other sources, such as the Strong Heart Study and the Indian Health Service, shows that smoking is a large contributor to heart disease, stroke, and cancer mortality in American Indian and Alaska Native populations (Mowery et al. 2015; Zhang et al. 2015). Lung cancer is the leading causes of cancer deaths in Alaska Native people (Nash et al. 2022). Another study showed significant heterogeneity in tobacco-caused cancers among Asian American and Native Hawaiian and Other Pacific Islander people (Medina et al. 2021). Each of these groups are unique, and additional data sources are needed to assess mortality within each group.

The aggregate group of the Asian American and Native Hawaiian and Other Pacific Islander population has historically had the lowest prevalence of smoking (see Chapter 2). However, rates of smoking differ within specific groups, and aggregation of data masks disparities in cancer incidence and mortality rates for such groups as Vietnamese, Chinese, Filipino, Japanese, Native Hawaiian, and Samoan people. An evaluation of the prevalence of smoking by ethnic population group that used data from the NHIS and the National Survey on Drug Use and Health revealed disparities in smoking within the Asian American and Native Hawaiian and Other Pacific Islander population (Martell et al. 2016). This study showed that the prevalence of smoking is historically higher among Korean and Vietnamese American people than among Chinese and Indian American people. Furthermore, differences in the prevalence of smoking by ethnic population and gender have been observed. For example, Gorman and colleagues (2014) reported that Vietnamese men were significantly more likely to smoke than Chinese men in models adjusted for various acculturation measures, but this association was not observed among women.

Other analyses have shown high SAFs of cancer deaths among specific Asian American and Pacific Islander groups, such as Korean men who live in California and the aggregate category of Asian and Pacific Islander or Hawaiian men and women who live in Hawaii (Leistikow et al. 2006). Similarly, lower than average prevalence of smoking among Hispanic people may mask differences in smoking and in the SAF of deaths by ethnic origin. For example, Puerto Rican and Cuban American people are more likely to smoke than Mexican American people (Martell et al. 2016).

Limitations

Smoking status in the NHIS-NDI LMF is assessed at only baseline, and thus a particular respondent’s smoking status recorded at the time of interview might not reflect that person’s status at time of death. For example, it is possible that observed deaths occurred among people who had quit smoking but were recorded as currently smoking at the time of their NHIS interview. Such cases would lead to an underestimation of the true RRs of mortality associated with current smoking among specific population groups. Conversely, the RR of mortality associated with former smoking may partially reflect the risk of those who recently quit smoking because of smoking-related illness, potentially inflating the risk associated with being a person who used to smoke.

This analysis does not separate estimates of mortality risk for people who quit smoking recently from those who quit smoking longer ago. The analysis by Jeon and colleagues (2023) found that the RR of all-cause mortality due to smoking for people who had quit smoking for longer periods was negatively associated with the time since quitting in groups defined by race and ethnicity and educational attainment; mortality rates for people who quit smoking 15 or more years ago were similar to those who had never smoked, particularly among those who were younger than 65 years of age. To partially address this limitation, follow-up for each respondent in the NHIS-NDI LMF is restricted to 10 years (an approach called right censoring). Although this approach does not completely address the potential for misclassification of smoking status, other longitudinal data sources that could address this issue may not be as representative of the U.S. population as the NHIS. Prevalence of smoking is only one factor that influences RR of death. For example, socioeconomic indicators; alcohol use; dietary behaviors; biological factors, such as metabolic pathways, inflammation, and pathophysiological processes; and other risk behaviors may influence the risk of mortality (Thun et al. 2000; National Institutes of Health State-of-the-Science Panel 2006; Orsi et al. 2010; Du et al. 2011; Jin et al. 2013; Deng et al. 2016; Singh and Jemal 2017; Milajerdi et al. 2018).

Additionally, the current analysis does not account for smoking intensity among people who currently smoked or who formerly smoked at baseline. However, in a recent analysis by Jeon and colleagues (2023), which stratified people by smoking intensity (as measured by the number of cigarettes smoked per day), RRs generally increased with higher levels of smoking intensity across population groups defined by race and ethnicity and by educational attainment. Notwithstanding, disparities in cancer incidence by race and ethnicity and smoking intensity have been observed. Specifically, data from the Multiethnic Cohort Study showed that Native Hawaiian people and Black people have higher risks for lung cancer than do White, Japanese American, and Hispanic or Latino people who smoke similar numbers of cigarettes; disparities were more pronounced among those who smoked 10 cigarettes per day than among those who smoked 35 cigarettes per day (Stram et al. 2019).

Several aspects of the methodology may have resulted in underestimates of RR and, thus, smoking-attributable mortality. First, the stratified nature of this analysis reduces the number of observable deaths in each relevant age, gender, and demographic category. When evaluating some racial and ethnic populations, this can translate into small numbers of observations. Nonsignificant RR estimates reported in Tables 6.36.6 may reflect insufficient power to detect statistical significance and may not be an accurate assessment of risk of mortality associated with current or former smoking.

Second, the long latency period between onset of smoking and subsequent smoking-related morbidity and mortality further limits the number of observable incidents in the NHIS-NDI LMF. With longer follow-up periods, RRs associated with death tend to increase. As such, restricting the follow-up period to 10 years (right censoring) may have resulted in an underestimate of RRs. The tradeoffs associated with methods to limit different forms of bias, while unavoidable, are important to acknowledge.

Another limitation is that RR estimates for some population groups exhibit wide CIs, which translates into wide ranges in the calculation of SAFs (Tables 6.76.9). Because SAFs for each population group of interest reflect the underlying prevalence and RRs specific to that group, direct comparisons between different smoking-attributable mortality estimates are not always appropriate.

The estimates of smoking-attributable mortality presented in this chapter include deaths for non-Hispanic Black, non-Hispanic White, and Hispanic adults only. Thus, overall estimates presented likely represent underestimates of the total smoking-attributable mortality for the United States. As such, the findings reported in this chapter should be considered only a first estimate of the contribution of smoking to the increased morbidity and mortality burdens faced by specific population groups in the United States; comprehensive data are critical for more refined estimates.

Finally, the estimates reported here focused on only cigarette-smoking-attributable mortality. Use of other tobacco products, including cigars, pipes, and smokeless tobacco, either alone or in combination with cigarette smoking and other tobacco products also contributes to mortality risk (Nonnemaker et al. 2014). Patterns of use of other combustible tobacco and smokeless tobacco products vary by race and ethnicity, level of educational attainment, geographic region, and other sociodemographic factors and may influence tobacco-related mortality across the U.S. population (Hirschtick et al. 2021).

Deaths Due to Exposure to Secondhand Tobacco Smoke Among Infants and Nonsmoking Adults, by Race and Ethnicity

The 2014 Surgeon General’s report included estimates from Max and colleagues (2012) of the number of deaths attributable to exposure to secondhand tobacco smoke among nonsmoking adults. The authors noted that 41,280 deaths among nonsmoking adults were attributable to exposure to secondhand tobacco smoke in 2006, including 33,950 deaths from coronary heart disease and 7,330 deaths from lung cancer. However, previous Surgeon General’s reports did not included estimates of deaths due to exposure to secondhand tobacco smoke in the United States by race and ethnicity. Leveraging the methodology developed by Max and colleagues (2012), the present report estimates deaths among infants for 2020 and among nonsmoking adults 18 years of age and older for 2019, overall and by race and ethnicity.

Detailed documentation of the methodology, including epidemiological formulas, is presented in Max and colleagues (2012). For newborns, estimates of exposure to secondhand tobacco smoke by race and ethnicity were obtained from National Vital Statistics Reports for 2020, the most recent year available at the time of analysis (Osterman et al. 2022). In brief, exposure to second-hand tobacco smoke among newborns was determined by whether the mother smoked anytime during pregnancy, as reported on the U.S. Standard Certificate of Live Birth. RRs of death due to exposure to secondhand tobacco smoke for sudden infant death syndrome and prenatal conditions were based on data from Dietz and colleagues (2010).

For adults 18 years of age and older, estimates of exposure to secondhand tobacco smoke were obtained from the NHANES during 2017 to March 2020 and based on serum cotinine (0.05–10.0 ng/mL). NHANES participants with missing serum cotinine measurements were excluded from the analysis. Following the methodology used in the study by Tsai and colleagues (2021), people who currently smoked and those who used any nicotinecontaining product, including nicotine replacement therapy, were excluded from the analysis. RRs of death from exposure to secondhand tobacco smoke for men and women were based on estimates from the 2006 Surgeon General’s report (USDHHS 2006) for coronary heart disease and a 2005 California Environmental Protection Agency report for lung cancer (Max et al. 2012, citing California Environmental Protection Agency 2005). The estimates of the prevalence of former, never, and current cigarette smoking were obtained from the 2019–2020 NHIS. The total number of deaths among infants less than 1 year of age (in 2020) and adults 18 years of age and older (in 2019) were from NCHS’s National Vital Statistics System, Multiple Causes of Death file, obtained from the CDC WONDER database.

Max and colleagues (2012) described the steps to estimate deaths among nonsmoking adults (people who never smoked and people who smoked in the past, combined), which were applied to produce the estimates for 2020. In short, deaths among nonsmoking adults were determined by (a) estimating the number of excess deaths attributable to current smoking; (b) subtracting these excess deaths attributable to active smoking from the total number of deaths among all people; and (c) apportioning the remaining deaths to people who did and did not smoke by applying the proportion of the population who did and did not smoke. The SAFs of deaths from exposure to secondhand tobacco smoke were estimated, then applied to total deaths among nonsmoking people who did not use nicotine-containing products in the previous 5 days for each condition category, by race and ethnicity.

Table 6.12 shows the percentage of newborn infants who were exposed to secondhand tobacco smoke in utero in 2020 and the percentage of nonsmoking men and women 18 years of age and older who were exposed to secondhand tobacco smoke from 2017 to March 2020, by race and ethnicity and for all races and ethnicities combined. Among all racial and ethnic groups, 5.5% of infants, 21.1% of men, and 19.3% of women were exposed to secondhand tobacco smoke. Among infants born in 2020, 1.4% of Hispanic, 4.5% of Black, and 8.1% of White infants were exposure to secondhand tobacco smoke in utero. Among women, exposure to secondhand tobacco smoke ranged from 14.5% among Hispanic women to 38.4% among Black women; 16.7% of White women and 24.4% of women of non-Hispanic Other races were exposed to secondhand tobacco smoke. Among men, exposure to secondhand tobacco smoke ranged from 18.2% for White men to 42.3% for Black men; 20.6% of Hispanic men and 24.7% of men of non-Hispanic Other race and ethnicity were exposed to secondhand tobacco smoke.

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Table 6.12

Prevalence of exposure to maternal smoking among newborn infants in utero and of cotinine-measured exposure to secondhand tobacco smoke among nonsmoking adults, by race and ethnicity.

Overall, these estimates suggest a decline in exposure to secondhand tobacco smoke since 2006, which is consistent with findings presented in Chapter 2 of this report. Specifically, Max and colleagues (2012) noted that in 2006, 13.2% of infants and 39.1% of adults 20 years of age (the minimum adult age included for that study) and older were exposed to secondhand tobacco smoke.

As shown in Table 6.13, an estimated 19,600 deaths attributable to exposure to secondhand tobacco smoke occurred among infants and nonsmoking adults in 2019 and 2020. Of these deaths, 70.7% (13,800) occurred among non-Hispanic White people, 19.1% (3,700) occurred among non-Hispanic Black people, 6.0% (1,200) occurred among Hispanic people, and 4.1% (800) occurred among non-Hispanic people of other races. In contrast, Max and colleagues (2012) found that in 2006, of the estimated 42,147 total deaths due to exposure to secondhand tobacco smoke, nonsmoking non-Hispanic White people accounted for 80% (33,746) of deaths, while non-Hispanic Black people accounted for 12.8% (5,410) of deaths, Hispanic people accounted for 4.1% (1,745) of deaths, and non-Hispanic, other racial and ethnic groups accounted for 3.0% (1,247) of deaths (Figure 6.1). Deaths among non-Hispanic Black, Hispanic, and other non-Hispanic racial groups accounted for a larger proportion of estimated deaths attributable to exposure to secondhand tobacco smoke in 2019 (adults) and 2020 (infants) (combined, 29.2%) compared with the proportion in 2006 (combined, 19.9%). Furthermore, among non-Hispanic White people, the estimated number of deaths attributable to exposure to secondhand tobacco smoke declined by nearly 60% from 2006 (n = 33,746) to 2019–2020 (n = 13,800). Smaller declines were observed among non-Hispanic Black people (by 31%; from 5,410 to about 3,700 deaths), Hispanic people (by 33%; from 1,745 to about 1,200 deaths) and non-Hispanic people from other races (by 35%; from 1,247 to about 800 deaths) during this period (Figure 6.1).

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Table 6.13

Estimated total number of deaths attributable to exposure to secondhand tobacco smoke among infants and nonsmoking adults, by cause, gender, and race and ethnicity, 2019 and 2020.

Illustration of the change in the estimated number of deaths due to exposure to secondhand tobacco smoke among infants and nonsmoking adults from 2006 to 2019 and 2020, as explained in detail in the narrative text.

Figure 6.1

Estimated number of deaths due to exposure to secondhand tobacco smoke among infants and nonsmoking adults, 2006 and 2019 and 2020. aData on deaths in 2006 among infants younger than 1 year of age and among adults, 20 years of age and older are from Max (more...)

The rate of death (per 100,000 population) due to exposure to secondhand tobacco smoke in 2019 was calculated from the estimated number of deaths due to exposure to secondhand tobacco smoke (Table 6.14). The denominator included adults 18 years of age and older who did not smoke. The total population of adults, averaged across 2019 and 2020 from the U.S. Census Bureau single-race population estimate, was obtained from CDC WONDER (CDC n.d.d). For each racial and ethnic group presented in Table 6.14, the prevalence of cigarette smoking was estimated from the 2019–2020 NHIS. The number of nonsmoking adults was estimated by multiplying the total adult population by the prevalence of never and non-current cigarette smoking. The rate of death was calculated as the estimated number of deaths due to exposure to secondhand tobacco smoke divided by the estimated population of nonsmoking adults.

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Table 6.14

Estimated number of deaths attributable to exposure to secondhand tobacco smoke and rates of death per 100,000 population among nonsmoking adults, by race and ethnicity, 2019.

Among all nonsmoking adults 18 years of age and older in 2019, an estimated 19,300 deaths were due to exposure to secondhand tobacco smoke, which equates to an estimated 8.7 deaths per 100,000 population (10.6 deaths per 100,000 men and 6.9 deaths per 100,000 women) (Table 6.14). Differences were noted by race and ethnicity. Although the greatest absolute number of deaths due to exposure to secondhand tobacco smoke occurred among White men and women, the highest population-specific death rates occurred among non-Hispanic Black men (16.4 deaths per 100,000 population) and non-Hispanic Black women (11.4 deaths per 100,000 population). The lowest rates of death due to exposure to secondhand tobacco smoke occurred among Hispanic adults: 3.9 deaths per 100,000 men and 2.1 deaths per 100,000 women.

Limitations

Similar to the analysis by Max and colleagues (2012), the current analysis is limited for several reasons. First, this analysis focused on deaths among nonsmoking people because it was challenging to separate the effects of exposure to secondhand tobacco smoke from the effects of active smoking and other tobacco product use on the health of people who use tobacco products. Nevertheless, there is no risk-free level of exposure to secondhand smoke, and such exposure harms health, including among people who smoke (USDHHS 2006; Max et al. 2012).

Second, although this analysis estimated deaths due to secondhand tobacco smoke exposure among infants, exposure to secondhand tobacco smoke was estimated only at birth based on the prevalence of self-reported maternal smoking while pregnant, as reported on the U.S. Standard Certificate of Live Birth. Thus, this proxy measure may underestimate total exposure to secondhand tobacco smoke among infants because of the potential for underreporting of maternal smoking behaviors at the time of birth or because this measure reflects only exposure in utero, as measured at the time of birth.

Third, the analysis is limited to conditions that are causally related to exposure to secondhand tobacco smoke for which there is a published estimate of the RR of death. Although the 2014 Surgeon General’s report concluded that exposure to secondhand tobacco smoke is a cause of stroke (USDHHS 2014), stroke deaths were not included in this analysis due to the lack of a published pooled estimate of the RR of stroke death from exposure to second-hand tobacco smoke. Furthermore, asthma deaths are not included in this analysis because Surgeon General’s reports have found suggestive but not sufficient evidence of a causal link between exposure to secondhand tobacco smoke and death from asthma (USDHHS 2014). Thus, these estimates may underestimate deaths attributable to exposure to secondhand tobacco smoke.

Fourth, although about 95% of examined adults, 18 years of age and older in the 2017 to March 2020 NHANES provided a blood specimen, about 12.5% of laboratory samples for all NHANES participants were not included in the analysis because the samples were missing a serum cotinine measurement (NCHS 2022). Additionally, similar to Max and colleagues (2012), variance was not estimated and thus no measures of precision are provided.

Fifth, the number of deaths attributable to exposure to secondhand tobacco smoke was estimated among nonsmoking adults (people who never smoked and people who smoked in the past, combined). Thus, some deaths among adults who smoked in the past and were exposed to secondhand tobacco smoke might be attributable to their previous smoking behaviors rather than to their exposure to secondhand tobacco smoke. However, because the RR of death for people who smoked in the past would be determined as the rate of death for people who smoked in the past who were exposed to secondhand tobacco smoke compared with people who smoked in the past who were not exposed to secondhand tobacco smoke, and because both of these groups were comprised of people who smoked at some point in their lives, the impact of smoking would likely dominate the comparison and the RR may be quite small.

Sixth, because RR estimates of death from exposure to secondhand tobacco smoke were not available for individual racial and ethnic population groups, the same RR estimates were used across all groups. Finally, as noted in the SAMMEC analysis described in this chapter, the small number of observed deaths in some racial and ethnic groups affected the ability to assess deaths for aggregate populations of Asian American people, Native Hawaiian and Pacific Islander people, American Indian and Alaska Native people, and people reporting multiple races, potentially masking racial and ethnic disparities in deaths due to exposure to secondhand tobacco smoke among these groups.

Summary of the Evidence

Despite continuing declines in the overall prevalence of smoking, cigarette smoking remains the leading cause of preventable death in the United States, exacting devastating tolls on the health of many U.S. population groups. Each year, on average, at least 473,300 people in the United States die from cigarette-smoking-attributable causes. Each year, on average, more than 400,000 non-Hispanic White, 50,000 non-Hispanic Black, and 15,000 Hispanic adults are estimated to die from diseases caused by smoking. There are large, absolute differences (i.e., magnitude of the difference) in the estimated number of smoking-attributable deaths among non-Hispanic White adults compared with non-Hispanic Black adults. However, smoking-attributable deaths represent a similar proportion of all deaths in these population groups (18% of all deaths for non-Hispanic Black adults and 20% of all deaths for non-Hispanic White adults). Furthermore, the proportion of all deaths attributable to smoking was about twice as high among non-Hispanic White and non-Hispanic Black adults as it was among Hispanic adults, among whom about 10% of all deaths were attributable to smoking during 2010–2018.

The 2014 Surgeon General’s report provided estimates of smoking-attributable mortality for the United States for 2005–2009, based on prevalence data for 1965–2011, concluding that smoking caused an estimated 439,000 deaths per year and exposure to secondhand tobacco smoke caused more than 41,000 deaths per year—a combined total of more than 480,000 deaths (USDHHS 2014). The present report estimated that cigarette smoking causes at least 473,000 deaths per year and exposure to secondhand tobacco smoke causes more than 19,000 deaths per year—totaling more than 490,000 deaths per year. This suggests that, although progress has been made in reducing deaths due to exposure to secondhand tobacco smoke and despite population-level declines in the prevalence of smoking, the overall death toll from smoking has not yet declined substantially during the twenty-first century.

The relative difference in annual estimates of smoking-attributable deaths between the 2014 Surgeon General’s report and the present report reflect population growth, particularly among older adults, during the period between the release of both reports. Although the prevalence of smoking among all U.S. adults has decreased, the prevalence of smoking has remained relatively stable among adults 65 years of age and older, an age group in which most smoking-related deaths occur (Jamal et al. 2015). Furthermore, the estimated number of smoking-attributable deaths presented in this report depends on the size, age, and demographic composition of the U.S. population. For example, the U.S. population is projected to increase to more than 435 million by 2050 and it will include increasing proportions of non-White racial and ethnic populations and people 65 years of age and older (Passel and Cohn 2008), which may change future comparisons of smoking-attributable mortality.

Also, although smoking cessation reduces the risk of mortality, many people who smoked in the past remain at higher risk of death compared with people who never smoked (Jha et al. 2013). As noted in the 2014 Surgeon General’s report, cross-sectional estimates of smoking attributable mortality may not accurately reflect the risks of previous cohorts of people who smoke when the prevalence of smoking changes over time. When the prevalence of smoking declines over time (as reported in Chapter 2), the SAMMEC methodology tends to underestimate the number of deaths caused by smoking (USDHHS 2014). In either case, the present report finds that the toll of cigarette smoking and exposure to secondhand tobacco smoke remains high, claiming nearly half a million lives per year.

Overall declines in exposure to secondhand tobacco smoke from 2006 to 2019–2020 have resulted in more than 22,500 fewer deaths attributable to exposure to secondhand tobacco smoke among infants and nonsmoking adults—a drop of more than 50% since 2006 (Max et al. 2012). Although all racial and ethnic groups experienced substantial declines in the number of deaths attributable to exposure to secondhand tobacco smoke, non-Hispanic White people accounted for 88.2% of the decline in such deaths (compared to 7.4% for non-Hispanic Black people, 2.5% for Hispanic people, and 1.9% for non-Hispanic people of other races). Furthermore, although the absolute number of deaths attributable to exposure to secondhand tobacco smoke was higher among non-Hispanic White adults than it is among adults in other racial and ethnic groups (due to the relative size of the non-Hispanic White population group), the population-specific death rate among non-Hispanic Black adults per 100,000 population is 1.4, 4.5, and 3.3 times higher than that for non-Hispanic White and Hispanic adults, and non-Hispanic adults of other races, respectively. These findings align with disparities in secondhand tobacco smoke protections and exposure to secondhand tobacco smoke; for example, Asian, Hispanic, and non-Hispanic White people are more likely than non-Hispanic Black people to live in jurisdictions with smokefree laws (Gonzalez et al. 2013; Hafez et al. 2019), and African American populations are disproportionately exposed to secondhand tobacco smoke (see Chapter 2).

Jha and colleagues (2013) reported that men and women who never smoked were about twice as likely than people who currently smoke to live to 80 years of age, with people who smoke dying, on average, a decade earlier than people who do not smoke. Most smoking-attributable deaths occur when people are in their late 60s and 70s—ages that are not attainable for people who have died early due to competing causes. RRs are a function of the mortality from smoking and nonsmoking-related causes, such that some population groups with higher competing causes of death may have lower RRs from current smoking. For example, estimated RRs of death from smoking are lower in Black adults, 35–54 years of age, than they are in White adults from the same age group. This may be attributable, in part, to a rate of death from all causes that is substantially higher among Black people, 18–34 years of age, (141.5 deaths per 100,000) than it is among White people from the same age group (100.3 deaths per 100,000) (RR = 1.41, 95% CI, 1.39–1.44). This is driven particularly by the rate of death from homicide, which is higher among Black people in this age group (47.2 deaths per 100,000) than it is among White people in this age group (5.5 deaths per 100,000) (RR = 8.59; 95% CI, 8.22–8.97) (Cunningham et al. 2017).

Similar counterintuitive findings are observed by level of educational attainment. For example, despite having a higher prevalence of smoking, people with lower educational attainment have lower estimated RR of death from smoking than people with higher educational attainment, although confidence intervals overlapped (Table 6.4). This is consistent with recent findings by Jeon and colleagues (2023), which also suggest higher competing causes of death among certain population groups (e.g., people with lower educational attainment), along with differences in other factors such as smoking intensity and duration, may result in lower RRs of death when comparing people who smoke to people who never smoked. In contrast, the findings note that people with higher educational attainment have fewer comorbidities or competing causes of death, which likely then results in higher RRs when comparing people who smoke to people who never smoked.

Because data in this report are limited, conclusions cannot be made about smoking-attributable deaths among aggregate groups of American Indian and Alaska Native people or Asian American and Native Hawaiian and Other Pacific Islander people. Studies show that there is significant heterogeneity in tobacco use behaviors and tobacco-caused morbidity and mortality among these groups, and risk for smoking-related outcomes relative to the number of cigarettes smoked per day is not the same across all groups (Haiman et al. 2006; Bliss et al. 2008; Medina et al. 2021; Nash et al. 2022; NCI n.d.). For example, risk of lung cancer is higher among African American and Native Hawaiian people who smoke no more than 10 cigarettes per day and among African American people who smoke 11–20 cigarettes per day than it is among their counterparts who are White, Japanese American, and Latino (Haiman et al. 2006; Stram et al. 2019). Thus, each group is unique, and additional data sources are needed to assess within-group mortality.

Although smoking influences the incidence of many chronic diseases, whether an individual survives a disease is also a function of other important factors—such as comorbidities; other individual risk behaviors; access to healthcare; and social and structural determinants of health, which are known to differ dramatically across social groups (Agency for Healthcare Research and Quality 2021). Thus, although the differences in mortality found in this chapter are strongly influenced by underlying differences in the prevalence of smoking and RRs, numerous other factors contribute to premature mortality.

This report finds that the toll of cigarette smoking and exposure to secondhand tobacco smoke remains high, claiming nearly half a million lives per year. Estimates of smoking-attributable mortality for select U.S. population groups are useful for public health decision makers, as the estimates highlight disparities that have not been addressed. However, gaps in available data for different population groups and sociodemographic factors such as income and access to healthcare may result in the under-representation of some groups in surveys or research studies. As such, multiple measures across the tobacco use spectrum—including initiation, use, cessation, exposure to secondhand tobacco smoke, and disease incidence and mortality; as well as intersectional demographic factors, including race and ethnicity, SES, sexual orientation and gender identity, and access to healthcare—can best inform the allocation of resources to eliminate tobacco-related disease and death. Both targeted and broad-scale tobacco control interventions are needed to reduce smoking-related health disparities and tobacco-related death and disease across diverse populations.

Simulation Modeling of Smoking Disparities

Simulation models—also known as computational models—have been used to show the relationship between tobacco control policies and patterns of tobacco use and their downstream health outcomes (Mendez et al. 2013; Holford et al. 2014b; Feirman et al. 2016, 2017; Levy et al. 2016, 2017b). These models can complement the analyses of smoking-attributable morbidity and mortality by (1) combining information from different sources and (2) including cross-sectional and longitudinal surveys and policy and health evaluation studies to examine how the effects of tobacco use and tobacco control policies could unfold over time. Numerous tobacco simulation models were reviewed in the 2014 Surgeon General’s report (USDHHS 2014) and by Feirman and colleagues (2016; 2017), but a limited number of tobacco models have considered explicitly groups that are disproportionately affected by tobacco-related health harms.

Chapter 12 of the NCI Tobacco Control Monograph 22 (NCI 2017a) discusses the SimSmoke disparity model—a modified version of the SimSmoke tobacco control simulation model—which was used to examine the potential effect of tobacco control policies on smoking and smoking-attributable deaths by SES in the United States. As illustrated in Chapter 2 of the current report, the prevalence of smoking is generally highest among people of lower SES—measured by poverty level and level of educational attainment—resulting in large disparities in the burden of tobacco-related disease and death by SES. Because levels of educational attainment are generally increasing in the U.S. population, the SimSmoke disparity model relies on income quintiles, which are a relative measure of SES and thus a more stable metric over time. Results of the SimSmoke disparity model are described next.

The SimSmoke model begins in 2006, when the prevalence of smoking among adults 18 years of age and older in the lowest income quintile was 30.2% for men and 22.7% for women. At that time, the prevalence of smoking among adults in the second lowest income quintile was 25.3% for men and 18.4% for women. The prevalence of smoking was higher in the lowest and second lowest income quintiles than it was in higher income quintiles. The model estimated that 119,526 people in the lowest income quintile and 95,986 people in the second lowest income quintile died prematurely from smoking in 2014 (NCI 2017a).

The SimSmoke disparity model showed that stronger tobacco control policies have the potential to reduce considerably the prevalence of smoking in lower income groups. The model simulated the specific effects of cigarette tax increases, smokefree policies, mass media antitobacco campaigns, marketing restrictions, health warnings, cessation treatment policies, and youth access policies for people in the two lowest income quintiles, taking into account moderating factors such as level of policy enforcement and intensity of publicity (NCI 2017a). The model simulated a status quo scenario by maintaining 2014 policy levels through 2064 and modeled the incremental effects of stronger policies implemented and maintained from 2015 through 2064 relative to the status quo. As shown in Table 6.15 (Parts A and B), raising the average cigarette tax by $3.00 per pack was projected to reduce the prevalence of smoking in the lowest quintile by 19.6% among men and by 19.5% among women, averting a total of 275,760 deaths from 2015 to 2064 (Table 6.16). For the second lowest quintile, the prevalence of smoking was similarly reduced, and 238,759 deaths were estimated to be averted over 50 years (NCI 2017a). All seven modeled policies were projected to reduce the prevalence of smoking and prevent smoking-attributable deaths in the lowest income quintile from 2015 to 2064, with the policy to raise the average cigarette tax to $3.00 per pack projected to have the largest effect (Table 6.15).

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Table 6.16

Smoking-attributable deaths among men and women in the lowest income quintile, according to the U.S. SimSmoke model.

The SimSmoke disparity model also evaluated the effects of implementing a combination of the individual policies, including a cigarette tax increase ($1.00, $2.00, or $3.00 per pack); comprehensive, well-enforced smokefree air laws (smoking banned in worksites, bars, restaurants, and other public places); high-intensity mass media antitobacco campaigns; comprehensive, well-enforced marketing restrictions; strong health warnings (on cigarette packages); cessation treatment policies; and strong youth access enforcement (to prohibit minors from accessing tobacco products). In the combined policy scenario that specifically included a $3.00 tax increase per pack of cigarettes, the modified SimSmoke model projected that, from 2015 to 2064, (a) the prevalence of smoking for people in the lowest income quintile would fall by 42.8% among men and by 43.7% among women and (b) a total of 845,401 smoking-attributable deaths would be averted (Tables 6.15 and 6.16). For the second lowest income quintile, the model projected that this same policy combination would avert 676,821 smoking-attributable deaths among men and women from 2015 to 2064 (NCI 2017a).

Furthermore, two U.S. simulation models examined populations with comorbidities and higher-than-average prevalences of smoking, specifically adults with depression (Tam et al. 2020) and adults living with HIV (Reddy et al. 2017). According to data from the 2017 National Survey on Drug Use and Health, the prevalence of smoking among people with depression was greater than 23%, relative to about 15% among people without depression (Weinberger et al. 2020). Among people living with HIV, the prevalence of smoking was greater than 40% (Mdodo et al. 2015; Asfar et al. 2021).

Tam and colleagues (2020) evaluated smoking disparities by mental health status, focusing on adults with a common mental health condition: major depression. They showed that in the absence of intervention, people with depression would remain disproportionately affected by tobacco-related mortality from 2018 to 2060. This model estimated that during this period, 484,000 smoking-attributable deaths and 11.3 million life-years would be lost among adults with major depression (Tam et al. 2020). Reddy and colleagues (2017) simulated lung cancer mortality among people living with HIV and showed that patients who adhere to antiretroviral therapy were 6 to 13 times more likely to die from lung cancer than from AIDS-related causes.

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Table 6.15

Status quo policies and SimSmoke-recommended policies: prevalence of smoking and percentage change among men and women, 18–85 years of age, in the lowest income quintile (percentages).

Investigators with the Cancer Intervention and Surveillance Modeling Network (CISNET) consortium generated smoking initiation, cessation, and intensity parameters that can be used to simulate long-term smoking and related health outcomes. For example, Holford and colleagues (2016) used age-period-cohort statistical models to estimate smoking history patterns over the life course among African American and White people in the United States. They found that the probabilities of smoking initiation and cessation and the intensity of cigarette smoking are historically lower among African American people than among White people. This translates into longer smoking durations but lower levels of cumulative exposure in pack-years for African American people. These age-period-cohort analyses and the resulting parameters for modeling have been extended for additional racial population groups by Hispanic origin (Meza et al. 2019), by levels of educational attainment (Cao et al. 2018), and by family income in relation to the federal poverty line (Jeon et al. 2019).

Numerous simulation models have used estimates of smoking from CISNET to evaluate long-term health outcomes at the population level (Jeon et al. 2012; Moolgavkar et al. 2012; Vugrin et al. 2015; Apelberg et al. 2018). The smoking histories modeled by CISNET can be modified in an interactive web based Tobacco Control Policy Tool (TCPT) (CISNET 2021) to estimate the impact of various tobacco control policies (e.g., enacting smokefree air laws, increasing cigarette taxes, raising the minimum age of legal access to tobacco products, increasing the level of expenditures for tobacco control programs, and adding graphic health warnings to cigarette packaging) on projections of adult smoking prevalence, number of life-years gained, and number of deaths avoided in the United States (Tam et al. 2018).

Simulation Modeling of the Prevalence and Attributable Mortality of Menthol Cigarette Use

Research shows that menthol cigarette use contributes to increased rates of smoking initiation and is associated with reduced smoking cessation among the general population and notably among Black people (Giovino et al. 2004; Ahijevych and Ford 2010; Delnevo et al. 2011; Levy et al. 2011a, b; Rath et al. 2015; Villanti et al. 2017, 2019, 2021; D’Silva et al. 2018; Nonnemaker et al. 2019; Azagba et al. 2020; Cwalina et al. 2020; Mantey et al. 2021; Mills et al. 2021; Center for Tobacco Products 2022). Further, research shows that the tobacco industry has heavily marketed menthol cigarettes to Black people, who are more likely to smoke menthol cigarettes than are people from other racial and ethnic groups who smoke (Tobacco Products Scientific Advisory Committee 2011; Alexander et al. 2016; Mendez and Le 2021; Levy et al. 2023; U.S. Food and Drug Administration n.d.). Therefore, the availability of menthol cigarettes in the marketplace differentially affects Black people compared with people from other races. This is true even though the majority of people who smoke menthol cigarettes are White, because White people make up the largest racial group in the United States (U.S. Census Bureau 2022). Thus, although a smaller proportion of White people who smoke report smoking menthol cigarettes, the total number of people who smoke menthol cigarettes is largest for White people.

As of February 2024, nearly 200 cities and counties and two states (Massachusetts and California) have implemented restrictions on the sale of menthol cigarettes and other flavored tobacco products (Campaign for Tobacco Free Kids 2024). Chapter 7 discusses studies that evaluate the impact of those subnational policies.

In the absence of experimental studies or an actual prohibition on menthol cigarettes at the federal level, simulation modeling can project the potential effects of a federal prohibition under reasonable scenarios on tobacco use and tobacco-related health outcomes. Models developed by Levy and colleagues (2011b; 2023), Mendez (2011), Le and Mendez (2021), and Mendez and Le (2021) have assessed the impact of menthol cigarettes on the prevalence of smoking and smoking-attributable deaths among Black or African American people and the total U.S. population. The model by Levy and colleagues (2011b) estimated the effects of a menthol ban, and the model by Mendez (2011) assessed the effects of menthol cigarettes on the population by contrasting a world with and without menthol cigarettes. In projecting future prevalence estimates for menthol and nonmenthol cigarette smoking, both models considered differential initiation and cessation rates among those who start with or become established menthol cigarette users. The results of various simulation models and their updates are summarized in Table 6.17 and discussed in this section.

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Table 6.17

Summary of simulation models estimating cumulative smoking-attributable deaths averted, if menthol cigarettes were banned, and premature (excess) deaths caused by menthol cigarettes: total population and Black or African American population, United States, (more...)

The SimSmoke model provided by Levy and colleagues (2011b) simulated the effect of a national-level menthol prohibition implemented in 2011 in three potential scenarios: (1) 10% of people who smoked menthol cigarettes permanently quit smoking, and 10% of those who would have initiated smoking with menthol cigarettes did not initiate smoking (10% change); (2) 20% of people who smoked menthol cigarettes quit, and 20.0% of those who would have initiated smoking with menthol cigarettes did not initiate (20% change); and (3) 30.0% of people who smoked menthol cigarettes quit, and 30.0% of those who would have initiated smoking with menthol cigarettes did not initiate (30% change). This model predicted that, in the absence of a federal menthol ban (i.e., the status quo), the prevalence of smoking would decline slowly and the proportion of remaining people who smoke menthol cigarettes would increase. However, in the presence of a prohibition on menthol cigarettes, the model projected greater reductions in the prevalence of smoking and fewer smoking-attributable deaths.

The SimSmoke model also showed that Black or African American people were projected to experience larger health gains from the menthol prohibition compared with the general population. Over a 40-year period (from 2010 through 2050), the 10% change scenario projected nearly a 5% relative reduction in the prevalence of smoking for the total population and a 9% relative reduction among Black or African American people (Levy et al. 2011b). Similarly, under the 20% and 30% change scenarios, the prevalence of smoking would decline by over 7% and nearly 10%, respectively, for all adults. However, these declines would be 17% and nearly 25%, respectively, among Black or African American people (Levy et al. 2011b).

FDA’s Tobacco Products Scientific Advisory Committee (TPSAC) completed a review of the scientific evidence related to menthol cigarettes in 2011. Based on smoking models reviewed, TPSAC specified model parameters to compare smoking outcomes under two scenarios, with and without the availability of menthol cigarettes (Mendez 2011; Tobacco Products Scientific Advisory Committee 2011). The model projected that more than 327,500 premature (or excess) deaths would be attributable to the availability of menthol cigarettes over a 40-year period (2010 to 2050), of which, more than 66,500 would be among Black or African American people (Mendez 2011). Mendez (2011) also conducted sensitivity analyses of the model parameters specified by the TPSAC on results for the total number of premature (or excess) deaths overall and with varying menthol-specific parameters in the model; results are included in summary Table 6.17.

The SimSmoke (Levy et al. 2011b) and Mendez (2011) models yield relatively consistent estimates for the general population. Both models find that menthol cigarettes disproportionately harm Black people, although, the Mendez (2011) model yields estimates of cumulative menthol-attributable deaths among Black people that are lower than estimates in the SimSmoke model under various scenarios.

The two models have limitations when viewed as forecasts of the effects of potential regulatory actions on menthol. Mendez (2011) modeled a hypothetical world without menthol cigarettes to estimate the present and future harms attributable to menthol cigarettes, but that study did not evaluate a specific model of menthol regulation and its consequences. Levy and colleagues (2011b) explicitly modeled the potential future effects of a national-level prohibition on menthol cigarettes under various hypothetical scenarios but did not estimate which, if any, of the scenarios was most likely. In addition, Levy and colleagues (2011b) did not consider the potential impact of mass media campaigns or increased access to cessation services when implementing a menthol prohibition. Chapter 7 describes implementation evaluations and considerations in more detail.

The Mendez model (2011) and the SimSmoke model (Levy et al. 2011b) were originally developed using data from before 2010, when smoking patterns were relatively stable and cigarettes were the overwhelmingly dominant form of tobacco product use. Since then, evidence on the relationship between the use of menthol cigarettes and smoking initiation and cessation has expanded (Villanti et al. 2017); Chapter 2 of this report provides data on prevalence and trends in menthol cigarette smoking by race and ethnicity and age.

To provide more contemporary estimates to address these developments, Le and Mendez (2021) updated the model Mendez developed for TPSAC (Mendez 2011) to estimate the burden of menthol cigarettes in the United States from 1980 to 2018. Their analysis suggests that the prevalence of smoking in the United States was 2.6 percentage points higher in 2018 than it would have been if menthol cigarettes had not been available from 1980 onward (13.7% versus 11.1%). Furthermore, the availability of menthol cigarettes was estimated to result in smoking initiation among 10.1 million people from 1980 to 2018, and 3 million years of life lost (Le and Mendez 2021). This model also estimated that 378,000 premature deaths occurred from 1980 to 2018 as a result of menthol cigarettes (Table 6.17), or approximately 9,900 premature deaths per year (Le and Mendez 2021).

Mendez and Le (2021) also used the updated model to examine the impact of menthol cigarettes on African American people from 1980 to 2018. Results from this study estimated that from 1980 to 2018, menthol cigarettes were responsible for initiation of smoking among 1.5 million African American people, 1.5 million years of life lost, and nearly 157,000 premature deaths among African American people. This study noted that, compared with estimates of the total menthol-related harm among the general population (Le and Mendez 2021), African American people experienced a disproportionate share of menthol-related harm with respect to these measures (15%, 50%, and 41%, respectively), as African American people constituted about 12% of the U.S. population during the study period.

Simulation Modeling of the Effects of Menthol Cigarette Bans Accounting for Use of E Cigarettes

Some developments in the tobacco product marketplace are not incorporated in the aforementioned models. The SimSmoke model (Levy et al. 2011b) and the Mendez models (Mendez 2011; Le and Mendez 2021; Mendez and Le 2021) did not incorporate (a) the combined use of conventional cigarettes with smokeless tobacco, cigars, hookah, or e-cigarettes (polytobacco use), or (b) the exclusive use of noncigarette tobacco products. Polytobacco use and exclusive use of noncigarette tobacco products are prevalent tobacco use behaviors among youth (Wang et al. 2019; Gentzke et al. 2020; Cho et al. 2021; Tam 2021) and adults, although exclusive use of noncigarette tobacco products is less common among adults (Lee et al. 2014; USDHHS 2014; Sung et al. 2016; Kasza et al. 2017; Hirschtick et al. 2021).

To partially address this gap, Levy and colleagues (2023) updated their original model to simulate the future benefit of a complete prohibition on menthol cigarettes and menthol cigars on the U.S. population from 2021 to 2060. This model accounts for the use of e-cigarettes both among people who smoke and do not smoke cigarettes and explores potential transitions between cigarette smoking and e-cigarette use in reaction to a menthol prohibition. The authors used the Smoking and Vaping Model (SAVM), which simulates population health effects of cigarette and e-cigarette use for specific birth cohorts. Levy and colleagues (2023) extended the SAVM to evaluate the use of nonmenthol and menthol cigarettes separately among people who (a) never used cigarettes or e-cigarettes, (b) smoked menthol cigarettes, (c) smoked nonmenthol cigarettes, (d) exclusively used e-cigarettes, (e) formerly smoked (menthol or nonmenthol cigarettes) but currently used e-cigarettes, (f) formerly smoked (menthol or nonmenthol cigarettes), and (g) formerly used e-cigarettes.

Compared with the status quo scenario in which a menthol prohibition was not implemented, the menthol prohibition scenario with implementation of the prohibition in 2021 was estimated to incur a relative reduction in the overall prevalence of smoking (menthol and nonmenthol cigarettes) by 14.7% by 2026 and by 15.1% by 2060 (Levy et al. 2023). This overall decrease reflects a sharp 92.5% relative reduction in menthol smoking by 2026 and a 96.5% relative reduction by 2060, but a smaller 47.4% relative increase in nonmenthol smoking by 2026 and a 58.0% relative increase by 2060. The menthol prohibition scenario was projected to increase exclusive e-cigarette use (including de novo, exclusive e-cigarette use and e-cigarette use among people who formerly smoked) from 3.5% in 2021 to 5.7% in 2026 and to 7.4% in 2060, equating to a 26.5% relative increase (compared with the status quo scenario) by 2060. Overall, the model estimated that the menthol prohibition scenario would result in more than 654,000 premature deaths averted and more than 11,300,000 life-years lost averted by 2060 compared with the status quo scenario. The authors concluded that their findings “strongly support the implementation of a ban on menthol in cigarettes and cigars” (Levy et al. 2023, p. 1). By way of limitation, the authors note that the model did not distinguish dual use of e-cigarettes and cigarettes from exclusive use of cigarettes, instead counting those who dual use as smoking only. Evidence suggests that dual use of electronic and combustible tobacco products may result in worse respiratory symptoms and greater exposure to toxicants than use of either product alone (Goniewicz et al. 2018; Reddy et al. 2021). Further, Levy and colleagues (2023) noted that the transition scenarios explored were based on mean results from an elicitation that relied on expert opinion, which differed regarding the extent of switching to e-cigarettes.

Levy and colleagues (2023) did not explore the public health impact of a complete menthol prohibition in cigarettes and cigars on the prevalence of smoking, deaths, and life-years lost among Black or African American people. However, Issabakhsh and colleagues (2023), using the SAVM and methodology similar to that of Levy and colleagues (2023), estimated the potential public health impact of a federal prohibition on menthol cigarettes among non-Hispanic Black people. The authors modeled various transitions among non-Hispanic Black adults, as noted by expert elicitation, following a federal prohibition on menthol cigarettes including switching to nonmenthol cigarettes, using illicit menthol cigarettes, switching to e-cigarettes, and quitting smoking. Under the menthol prohibition scenario, the model projected, among non-Hispanic Black adults, the prevalence of (a) smoking menthol cigarettes would decline from 12.1% in 2021 to 0.7% in 2026 and to 0.2% in 2060 and (b) smoking nonmenthol cigarettes would increase from 2.2% in 2021 to 6.7% in 2026, followed by a decline to 3.6% in 2060. Compared with the status quo scenario, a menthol cigarette prohibition implemented in 2021 is projected to result in relative reductions in overall (menthol and nonmenthol) cigarette smoking among non-Hispanic Black adults of 35.7% in 2026 and 25.3% in 2060, but nonmenthol cigarette smoking and e-cigarette use were projected to increase over this period. Even so, the model projected that nearly 256,000 premature deaths and 4 million life-years lost would be averted among non-Hispanic Black adults under the menthol prohibition scenario relative to the statusquo scenario from 2021 to 2060 (Issabakhsh et al. 2023).

Compared to the results of the SAVM for the general population (relative to the status quo) as reported by Levy and colleagues (2023), the findings reported by Issabakhsh and colleagues (2023) for the SAVM for non-Hispanic Black people suggest that a menthol prohibition would result in several strong impacts (relative to the status quo) among non-Hispanic Black adults:

  • Overall reduction in the prevalence of smoking: 25.3% through 2060 in the SAVM for non-Hispanic Black people versus 15.1% through 2060 in the SAVM for the general population;
  • Reductions in cumulative averted deaths from 2021 to 2060: 18.5% in the SAVM for non-Hispanic Black people versus 4.6% in the SAVM for the general population; and
  • Relative reductions in cumulative life-years lost from 2021 to 2060: 22.1% in the SAVM for non-Hispanic Black people vs. 7.9% in the SAVM for the general population.

Projections of averted deaths and life-years lost among non-Hispanic Black adults are approximately one-third of those projected by SAVM for the general population, despite the non-Hispanic Black population making up only 13.6% of the overall U.S. population in 2021. Thus, the authors note that a national menthol prohibition would result “simultaneously in considerable health gains and in reductions in health disparities between the non-Hispanic [B]lack and the rest of the US population” (Issabakhsh et al. 2023, p. 1). Findings were subject to the same limitations as those in the study by Levy and colleagues (2023); that is, dual use was not included in the model, and the effects of menthol prohibition on smoking and vaping initiation and cessation were based on expert elicitation. Furthermore, Issabakhsh and colleagues (2023) noted that the SAVM for non-Hispanic Black people did not distinguish between health outcomes among people who exclusively smoked menthol cigarettes and transitioned to cigar use as a result of the menthol prohibition.

Additional Considerations for Modeling Changes in the Flavored Tobacco Product Marketplace

Noncigarette tobacco products—such as little cigars, smokeless tobacco, and e-cigarettes—are available in menthol and other flavors (Buu et al. 2018; Russell et al. 2018; Schneller et al. 2018; Webb Hooper and Smiley 2018; Zare et al. 2018). These flavored tobacco products may (a) increase the likelihood of future cigarette smoking, (b) be used in conjunction with menthol and nonmenthol cigarettes (i.e., dual use), or (c) be used as substitutes for menthol cigarettes by people who are attempting to quit cigarettes or quit all tobacco products. Simulation models have explored scenarios involving multiple tobacco products (Kalkhoran and Glantz 2015; Cherng et al. 2016; Levy et al. 2017a, 2018, 2023; National Academies of Sciences, Engineering, and Medicine 2018; Warner and Mendez 2018; Brouwer et al. 2020; Mendez and Warner 2020; Niaura et al. 2020). However, none have specifically considered menthol flavoring in e-cigarettes, dual use of e-cigarettes and cigarettes, or differences in patterns of use by race and ethnicity or SES.

The magnitude of the effects of a federal prohibition on menthol cigarettes and flavored cigars would depend on (a) the proportion of people who use cigarettes who transition in whole or in part to other tobacco products and (b) whether such a flavor prohibition would be applied to other tobacco products. If a flavor prohibition was applied to cigarettes and cigars only, the impact of other menthol flavored tobacco products (e.g., e-cigarettes) remaining on the market on important outcomes—such as smoking cessation, complete tobacco product cessation, and tobacco product initiation—is unknown. It is also unclear if these effects would vary by race and ethnicity or SES. As of February 2024, two states (Massachusetts and California) prohibit the sale of all flavored tobacco products, including menthol cigarettes, cigars, and e-cigarettes (Campaign for Tobacco Free Kids 2024). Evaluations of the impacts of state-level flavor restrictions on the use trajectories and variations by race and ethnicity or SES can further elucidate the effects of such restrictions among various population groups.

Future Research Considerations for Simulation Modeling

Simulation models (a) make it possible to examine the potential role of various tobacco control policies in reducing rates of smoking among population groups that are at higher risk and (b) are well suited for evaluating complex social problems that may have unexpected consequences or that may vary with time. Future simulation models that evaluate the impact of specific policies on disparities in smoking could be designed to integrate the effects of noncigarette tobacco products with patterns of smoking. These models could consider whether individuals transition from cigarettes to cigars, smokeless tobacco, or heated tobacco products or vice versa; to dual use; or to complete cessation of all tobacco products.

Thus far, models of smoking in the United States that account for differences in the population by race and ethnicity and SES have been mostly compartmental (macro-level) models that examine trends in aggregate population groups, with a limited number of population categories. To account for diverse populations defined by race and ethnicity, SES, or other sociodemographic factors, as well as the specific patterns of tobacco use within these variables, individual-level models may be useful because they avoid what is known as the “state explosion” problem—that is, the need to dramatically increase the number of model compartments to correspond with the increased number of population characteristics (e.g., race and ethnicity or education) (Siebert et al. 2012).

Models that focus on behavior changes at the individual level—such as microsimulation, agent-based models, or social network models—could be used to show the impact of social stratification on outcomes for the prevalence of smoking (Chao et al. 2015). These types of models could be used to help assess underlying patterns of tobacco use and tobacco-related health disparities for people of lower SES, racial and ethnic groups, and other populations such as people with two or more health conditions at once. The models could also be used to help evaluate the impact of tobacco control policies and regulations on tobacco use patterns and tobacco-related health equity.

Although findings from simulation models are sensitive to the assumptions used and the overall availability, timeliness, and representativeness of the data put into the model, simulation models are increasingly recognized as important tools for evaluating the effects of tobacco use and tobacco control interventions across diverse populations (Ashley et al. 2014; Walton et al. 2015; Backinger et al. 2016). Thus, future models developed for this purpose should be designed with several research considerations in mind.

Data Gaps in Simulation Modeling

Data sources used as model inputs may not be representative of all study populations of interest. In particular, national data are often limited and provide insufficient sample sizes to (a) estimate morbidity and mortality among racial and ethnic groups; (b) investigate the intersection of these groups with sexual orientation, gender identity, level of educational attainment, and poverty status; (c) provide detailed data on tobacco use patterns, including use of noncigarette combustible tobacco products such as cigars; and (d) estimate the health effects of tobacco use (which are usually parameterized and incorporated into models as RRs) and policy effects for specific groups. For instance, historical models of smoking (Holford et al. 2014a,b, 2016; Levy et al. 2016) have relied heavily on RR estimates from the American Cancer Society’s Cancer Prevention Study I and Study II. Data collected for these studies came mostly from White, college-educated samples (Rosenberg et al. 2012). These estimates have been updated to include data from five large prospective cohorts (Thun et al. 2013a,b; Carter et al. 2015) and more recent national surveys (Christensen et al. 2018; Choi et al. 2019; Inoue-Choi et al. 2019; Jeon et al. 2023). However, a lack of data on diverse groups remains. The RR estimates presented for different sociodemographic groups in this chapter are an important addition to the literature that can enable the development of further simulation models of smoking-related disparities. Additional data on health effects are critical to investigate the impact of cigarette and noncigarette tobacco products on populations disproportionately affected by tobacco harms.

Detailed data that go far beyond levels of the prevalence of smoking are also needed to determine tobacco use patterns for all relevant sociodemographic groups and other population groups that are disproportionately affected by tobacco use, such as people with mental health conditions. The average age at smoking initiation or smoking cessation or the level of smoking intensity may be lower or higher in specific population groups compared with the general population, as is the case for Black people and people without a college degree or above, respectively (Siahpush et al. 2010). For example, lesbian, gay, bisexual, and transgender people smoke at disproportionately high rates compared with the rest of the population (Lee et al. 2009) and represent an understudied group (Institute of Medicine 2011).

Although models for these population groups could draw from studies conducted at the state and local levels, models at the national level may be limited because nationally representative inputs from national health surveys have only begun to include questions about sexual orientation and gender identity relatively recently. For example, when the NHIS began asking about sexual orientation in 2013, only two other national-level surveys (the National Health and Nutrition Examination Survey and the National Survey of Family Growth) had included this measure (Dahlhamer et al. 2014). NHIS only began asking about gender identity in 2022 (NCHS 2023). Future national surveys should be sufficiently powered to collect detailed information about tobacco use in these and other understudied population groups. This information is needed to facilitate the development of simulation models that address tobacco-related health disparities.

State- and local-level data may provide more robust estimates for small population groups. To date, national-level data have not provided the estimates needed for different racial and ethnic groups, because non-White population groups collectively represented about 39% of the U.S. population as of 2020 (Jones et al. 2021). Sampling methods for national-level studies aim to generate nationally representative samples but may not consider the sample sizes needed to calculate robust estimates among specific population groups. The lack of data at the national level has repeatedly resulted in conclusions that the sample sizes are insufficient to examine outcomes for certain population groups. While pooling data from multiple years is one technique to increase sample size, statistical power, and precision, pooling may mask changes among population groups over time because it requires estimates to be interpreted as the average over the time period being pooled. As such, national surveillance data systems should seek to improve methods to collect more robust data on different population groups. It is also important to continue to examine alternative ways of collecting and analyzing data from diverse groups. Numerous models exist, particularly for American Indian and Alaska Native groups, where various researchers have used different datasets to understand regional differences in smoking and tobacco-caused cancers (Wiggins et al. 2008; Torre et al. 2016).

Population groups with two or more behavioral or physical health conditions at once present distinct modeling challenges. Data are important to understand how concurrent behaviors and conditions may interact with smoking to produce health outcomes that may either increase or reduce disparities for these populations. For instance, smoking prevalence and intensity have been shown to be higher among people with mental health conditions compared with people without mental health conditions (Lipari and Van Horn 2017). Models that simulate these populations should account for the potential interactions of smoking with other diseases such as HIV (Mdege et al. 2017) or mental health conditions (Hassmiller 2006; Prochaska et al. 2017; Reddy et al. 2017; Tam et al. 2020).

Policy Effects by Sociodemographic Group

Few simulation modeling studies have examined the impact of smoking on illness, healthcare costs, or lost earnings across diverse populations. Moreover, information about the specific effects of different tobacco control policies and regulations on smoking patterns for different sociodemographic or at-risk population groups is limited. In recent decades, evidence has been growing on the effectiveness of various tobacco control policies on disparities in smoking, discussed in detail in Chapter 7. Regardless, understanding is limited by (a) the scope of populations that are investigated; (b) the relative lack of focus on the outcomes of initiation and cessation, which are important to simulation modeling efforts; and (c) the need for additional analyses using more up-to-date, nationally representative data.

Federal agencies recognize that limited information is available about policy effects by sociodemographic group, and they encourage and invest in research funding in this area (NCI 2017b; CDC 2021, 2023a,b; National Institutes of Health n.d.). Future research could examine the impact of smoking on morbidity, disability, healthcare costs, years of potential life lost, and productivity losses among various population groups. Results from this research could enhance knowledge about the impact of tobacco control policies on these important populations. Simulation modelers can build on this work by integrating this information into their models as it becomes available.

Heterogeneous Groups

Models assessing heterogeneous populations should consider the potential for heterogeneity even within sociodemographic groups. For example, although aggregate Hispanic/Latino and Asian populations have a lower-than-average prevalence of smoking overall, heterogeneity may mask differences related to country of origin and level of acculturation. Both groups represent diverse populations whose overall health profiles mask interethnic disparities. For example, the prevalence of smoking and frequency of smoking are significantly higher among Puerto Rican and Cuban American people than among Mexican American people (Blanco et al. 2014; Gorman et al. 2014). Differences by sex within and across ethnic groups also matter. For example, Vietnamese men are far more likely to smoke than Chinese men, but this pattern is not apparent in comparisons of Vietnamese and Chinese women (Gorman et al. 2014). In addition, longer duration of U.S. residence is associated with increased smoking within Asian and Hispanic immigrant populations. Although efforts should be made to identify inputs appropriate for each modeled population, efforts to simplify assumptions used in each model should be informed by existing literature about patterns of tobacco use because they vary across and within sociodemographic groups.

Changing Demographics

The overall composition of the U.S. population is changing. To obtain a more complete picture of the complex identities of the U.S. population, questions assessing Hispanic origin and each race group were improved in the 2020 U.S. Census. These improvements included having dedicated write-in response options, allowing respondents to provide additional details to the questions assessing Hispanic origin and race (Marks and Rios-Vargas 2021). These design improvements will likely lead to changes in national estimates of the prevalence of smoking as they resulted in differences in overall racial distributions as compared with the 2010 Census (Jensen et al. 2021). For instance, previous research showed that the rising proportion of Hispanic people in the U.S. population, a group with a lower-than-average prevalence of smoking, was a significant contributor to overall declines in the prevalence of smoking in the United States from 1980 to 2010 (Tam et al. 2014).

The aggregate group of Asian American people represent the fastest growing racial group in the United States (Hoeffel et al. 2012; Budiman and Ruiz 2021a). Although the prevalence of smoking is lower among Asian American people, as an aggregate group, than among White or Black people (Cornelius et al. 2022), past studies indicate that rates of smoking vary within aggregate populations (Li et al. 2013; Martell et al. 2016). Differences in the prevalence of smoking will depend on which Asian population groups are increasing in the United States, by gender, geographic region, level of educational attainment, and income. Chinese, Indian American, Filipino, Vietnamese, Korean, and Japanese people were the Asian groups that accounted for most of the Asian population in the United States in 2019 (Budiman and Ruiz 2021b). These groups have different smoking profiles and disease risk and also differ widely with respect to level of educational attainment, English proficiency, income, and recency of immigration, which could influence future prevalence of smoking among the aggregate population of Asian American people (Budiman and Ruiz 2021b).

Other changing demographics, including the aging of the overall population and greater racial and ethnic diversity in younger population groups (Rabe and Jensen 2023), are likely to influence statistics on tobacco use and how models incorporate these statistics to make future health projections. Developers of models that aim to represent the changing demographics of the U.S. population should, where possible, draw from data sources that will allow such representativeness, such as migration trend estimates.

Evolving Tobacco Landscape

As noted previously, most tobacco simulation models of smoking fail to consider simultaneous or polyuse of tobacco products (Lee et al. 2014; USDHHS 2014; Sung et al. 2016; Kasza et al. 2017; Hirschtick et al. 2021). Simulation models of smoking should incorporate data on noncigarette tobacco products such as e-cigarettes, cigars, smokeless tobacco, hookah, nicotine pouches, and heated tobacco products. Among youth, use of e-cigarettes in isolation and in combination with other tobacco products has become increasingly common, even as the use of combustible tobacco products among youth declines (Wang et al. 2019; Cho et al. 2021; Tam 2021). Additionally, adults use e-cigarettes concurrently with cigarettes more than other tobacco products (Mattingly et al. 2021). Patterns of polytobacco use vary by race and ethnicity, SES, and other sociodemographic factors, which poses a challenge for studies that aim to evaluate multiproduct use across multiple subpopulations.

Simulating the use of multiple tobacco products using the traditional compartmental or macro-level models may be challenging because having an increasing number of compartments for different categories of tobacco use increases the complexity and computational needs of macro-level models (Siebert et al. 2012). Individual-based models, such as agent-based and network-based models, can apply simple rules to individual behaviors and explore how social interactions and social segregation could influence polytobacco use, downstream population-level health outcomes, and tobacco-related disparities. Individual-based models are especially applicable for research that investigates neighborhood contexts and the transmission of tobacco use behaviors among adults and adolescents (Lakon et al. 2010; Luke et al. 2017). By integrating information about diversity in the study population and in the tobacco product marketplace, simulation models can assess the potential health consequences of various interventions, inform future decision making, and increase the likelihood that future public health aims will be met.

Summary of the Evidence and Implications

Simulation models can evaluate the effects of large-scale interventions on smoking-attributable morbidity and mortality and on disparities in tobacco use across various population groups. Few existing simulation models of smoking and of use of other tobacco products consider patterns of use by race, ethnicity, SES, or other demographic factors. Even fewer models explicitly measure disparities using recommended measures of health disparities (Harper and Lynch 2005) or evaluate whether disparities may change as smoking patterns evolve. Even so, the modeling research available to date demonstrates the usefulness of models in assessing patterns of smoking over time and projecting long-term health outcomes as they vary across populations. Future modeling efforts would benefit greatly from the following:

  • Detailed data about historical patterns of smoking,
  • Continued examination of the differential effects of tobacco control policies on specific sociodemographic groups,
  • Consideration of the heterogeneity of racial and ethnic population groups within and across populations,
  • Adjustments for shifts over time in the composition of populations, and
  • Information about the use of various noncigarette tobacco products and the behaviors of specific sociodemographic groups in transitioning to those products or dual use of cigarette and noncigarette products.

Simulation models can be developed following best practices regarding model specification and structure such as those recommended by ISPOR (formerly the International Society for Pharmacoeconomics and Outcomes Research) and the Society for Medical Decision Making’s Modeling Good Research Practices Task Force (Briggs et al. 2012; Caro et al. 2012; Eddy et al. 2012; Karnon et al. 2012; Pitman et al. 2012; Roberts et al. 2012; Siebert et al. 2012) to readily integrate new evidence as it emerges and explore a wide range of future health interventions that will alleviate the burden of tobacco use and its associated morbidity and mortality in populations at greater risk. The impact of modeling studies in this area could be enhanced by (a) adding recommended measures of health disparities into their analyses and (b) evaluating how interventions and changes in tobacco use behaviors could widen or narrow tobacco-related health disparities over time.

Conclusions

  1. Smoking is the primary cause of lung and bronchus cancers—the leading cause of cancer death in the United States. Recent declines in the lung and bronchus cancer death rate have occurred among both men and women. Among men, the death rate for lung and bronchus cancer is highest among Black men, followed by White men, American Indian and Alaska Native men, Asian and Pacific Islander men, and Hispanic men. Among women, the death rate for lung and bronchus cancer is highest among White women, followed by American Indian and Alaska Native women, Black women, Asian and Pacific Islander women, and Hispanic women.
  2. Cigarette smoking is a primary cause of COPD and the primary risk factor for the worsening of COPD. The overall prevalence of COPD is highest among American Indian and Alaska Native adults and lowest among Asian adults. There is a clear socioeconomic gradient for COPD prevalence and mortality, with higher prevalence and mortality occurring among people with lower income and lower educational attainment.
  3. Cigarette smoking and exposure to secondhand tobacco smoke have adverse effects on overall cardiovascular health and cause cardiovascular disease. Among men, the prevalence of cardiovascular disease in 2017–2020 was highest among non-Hispanic Black (11.3%) and non-Hispanic White (11.3%) men, followed by Hispanic men (8.7%) and non-Hispanic Asian men (6.9%). Among women, the prevalence of cardiovascular disease was highest among non-Hispanic Black women (11.1%), followed by non-Hispanic White (9.2%), Hispanic (8.4%), and non-Hispanic Asian (4.9%) women.
  4. From 2010 to 2018, an estimated 4.26 million smoking-attributable deaths occurred among non-Hispanic Black, Hispanic, and non-Hispanic White adults in the United States. Among those groups, at least 473,000 cigarette smoking-attributable deaths are estimated to have occurred each year.
  5. Smoking causes about 1 in 5 deaths among non-Hispanic White and non-Hispanic Black people and about 1 in 10 deaths among Hispanic people.
  6. An estimated 19,600 deaths attributable to exposure to secondhand tobacco smoke occurred among nonsmoking people in the United States based on data from 2019 and 2020. Deaths attributable to exposure to secondhand tobacco smoke have declined considerably since 2006, but this is largely due to the declines in death observed among non-Hispanic White people. Declines occurred at lower rates during this period among non-Hispanic Black, Hispanic, and other non-Hispanic racial groups.
  7. Simulation models can be useful tools to project the potential effects of large-scale interventions on smoking-attributable morbidity and mortality and on disparities in tobacco use across various populations. Future modeling efforts would benefit from (a) more detailed data on patterns of smoking and the use of noncigarette tobacco products; and (b) more robust data for racial and ethnic groups; minoritized sexual orientation and gender identity groups; urban and rural communities; and other focused populations.
  8. Aggregation of data on tobacco product use, disease incidence, and mortality may mask disparities within population groups, such as within Asian American and Native Hawaiian and Other Pacific Islander groups. Disaggregation of data reporting and oversampling among disparate populations will foster greater understanding of tobacco-related health disparities.

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Chapter 6. Appendix

Appendix 6.1. Population-Level Estimates of the Prevalence of Smoking Statuses by Demographic Variables

Table 6A.1Cigarette smoking status (weighted %) by gender, race and ethnicity, and age group; National Health Interview Survey (NHIS), 2010–2018

Gender, race and ethnicity, and age groupCurrent smoking (%)Former smoking (%)Never smoking (%)
Men
 Hispanic
  35–5415.419.964.7
  55–6414.532.952.6
  65–7413.042.244.8
  ≥757.148.944.0
 Non-Hispanic Black
  35–5423.413.662.9
  55–6425.126.948.0
  65–7418.442.938.7
  ≥7510.849.839.3
 Non-Hispanic White
  35–5422.224.053.8
  55–6419.334.146.6
  65–7412.149.538.4
  ≥755.857.636.7
Women
 Hispanic
  35–548.910.181.0
  55–649.017.873.2
  65–745.719.774.6
  ≥753.617.578.9
 Non-Hispanic Black
  35–5416.39.174.6
  55–6417.021.061.9
  65–7410.825.663.6
  ≥757.229.663.2
 Non-Hispanic White
  35.5421.521.457.1
  55.6416.128.555.4
  65.7410.935.154.1
  ≥755.835.159.1

Source: NHIS public use dataset, 2010–2018.

Table 6A.2Cigarette smoking status (weighted %) by gender, level of educational attainment, and age group; National Health Interview Survey (NHIS), 2010–2018

Gender, level of educational attainment, and age groupCurrent smoking (%)Former smoking (%)Never smoking (%)
Men
 ≤8th grade
  35–5422.021.157.0
  55–6422.733.943.4
  65–7420.544.934.6
  ≥759.456.634.0
 9th–12th grade, no diploma
  35–5444.118.937.1
  55–6438.336.125.6
  65–7421.552.526.0
  ≥7510.160.729.2
 High school diploma or GED
  35–5430.722.546.8
  55–6428.033.838.1
  65–7416.251.232.6
  ≥757.359.533.2
 Some college, no degree
  35–5422.025.552.5
  55–6420.436.643.0
  65–7414.051.434.6
  ≥756.157.636.2
 ≥College degree
  35–547.618.973.4
  55–647.728.763.6
  65–746.042.951.0
  ≥753.048.848.2
Women
 ≤8th grade
  35–5411.96.881.3
  55–6414.113.572.4
  65–749.219.271.7
  ≥755.921.273.0
 9th–12th grade, no diploma
  35–5433.613.053.4
  55–6433.323.243.5
  65–7418.830.650.7
  ≥7511.031.157.9
 High school diploma or GED
  35–5427.516.855.7
  55.6420.725.553.8
  65.7412.232.455.4
  ≥755.932.062.2
 Some college, no degree
  35.5420.719.959.4
  55.6416.528.155.3
  65.7411.033.855.2
  ≥755.137.457.5
 ≥College degree
  35.547.216.276.6
  55.646.025.368.7
  65.744.731.064.3
  ≥753.133.863.0

Source: NHIS public use dataset, 2010–2018.

Note: GED = General Educational Development.

Table 6A.3Cigarette smoking status (weighted %) by gender, geographic region, and age group; National Health Interview Survey (NHIS), 2010–2018

Gender, geographic region, and age groupCurrent smoking (%)Former smoking (%)Never smoking (%)
Men
 Northeast
  35–5418.723.358.0
  55–6416.531.951.6
  65–7410.249.240.6
  ≥755.851.342.8
 Midwest
  35–5423.722.653.7
  55–6422.233.544.3
  65–7413.549.037.6
  ≥756.458.335.3
 South
  35–5422.620.257.3
  55–6420.832.446.8
  65–7413.948.437.7
  ≥757.155.737.2
 West
  35–5416.922.460.7
  55–6416.334.549.2
  65–7411.545.343.3
  ≥755.456.038.6
Women
 Northeast
  35–5416.319.364.4
  55–6414.429.056.6
  65–749.535.255.3
  ≥755.433.061.5
 Midwest
  35–5422.518.958.6
  55–6417.027.056.0
  65–7411.832.255.9
  ≥756.732.560.8
 South
  35–5418.715.366.0
  55–6416.323.959.9
  65–7410.429.360.3
  ≥755.531.962.6
 West
  35–5412.415.871.8
  55.6411.924.263.8
  65.748.331.360.5
  ≥755.033.361.7

Source: NHIS public use dataset, 2010–2018.

Footnotes

1

Corresponding confidence intervals were not available for estimates presented in American Lung Association (n.d.).

2

Corresponding confidence intervals for the prevalence of cardiovascular disease overall and by race and ethnicity were unavailable (Tsao et al. 2023)

3

Gender was categorized as male or female only. Other gender identities, including nonbinary, were not assessed in the NHIS during this period.

*

URL was active on the access date shown in the reference entry but was no longer active when this Surgeon General’s report was released.

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