recommendation about smoking essay

Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence (2010)

Chapter: 8 conclusions and recommendations, 8 conclusions and recommendations.

In this report, the committee has examined three relationships in response to its charge (see Box 8-1 for specific questions):

The association between secondhand-smoke exposure and cardiovascular disease, especially coronary heart disease and not stroke (Question 1).

The association between secondhand-smoke exposure and acute coronary events (Questions 2, 3, and 5).

The association between smoking bans and acute coronary events (Questions 4, 5, 6, 7, and 8).

This chapter summarizes the committee’s review of information relevant to those relationships; presents its findings, conclusions, and recommendations on the basis of the weight of evidence; and presents its responses to the specific questions that it was asked in its task.

SUMMARY OF REPORT

Exposure assessment.

To determine the effect of changes in exposure to secondhand smoke it is necessary to quantify changes in epidemiologic studies. Airborne measures and biomarkers of exposure to secondhand smoke are available; they are complementary and provide different information (see Chapter 2 ). Biomarkers (such as cotinine, the major proximate metabolite of nicotine) in-

tegrate all sources of exposure and inhalation rates, but cannot identify the place where secondhand-smoke exposure occurred and, because of a short half-life they reflect only recent exposures. Airborne measures of exposure can demonstrate the contribution of different sources or venues of exposure and can be used to measure changes in secondhand-smoke concentrations at individual venues, but they do not reflect the true dose. Airborne concentration of nicotine is a specific tracer for secondhand smoke. Particulate matter (PM) can also be used as an indicator of secondhand-smoke exposure, but because there are other sources of PM it is a less specific tracer than nicotine. The concentration of cotinine in serum, saliva, or urine is a specific indicator of integrated exposure to secondhand smoke.

Although in most of the smoking-ban studies the magnitude, frequency, and duration of exposures that occurred before a ban are not known, monitoring studies demonstrate that exposure to secondhand smoke is dramatically reduced in places that are covered by bans. Airborne nicotine

and PM concentrations in regulated venues such as workplaces, bars, and restaurants decreased by more than 80% in most studies; serum, salivary, or urinary cotinine concentrations decreased by 50% or more in most studies, probably reflecting continuing exposures in unregulated venues (for example, in homes and cars).

Pathophysiology

The pathophysiology of the induction of cardiovascular disease by cigarette-smoking and secondhand-smoke exposure is complex and undoubtedly involves multiple agents. Many chemicals in secondhand smoke have been shown to exert cardiovascular toxicity (see Table 3-1 ), and both acute and chronic effects of these chemicals have been identified. Experimental studies in humans, animals, and cell cultures have demonstrated effects of secondhand smoke, its components (such as PM, acrolein, polycyclic

aromatic hydrocarbons [PAHs], and metals), or both on the cardiovascular system (see Figure 3-1 for summary). Those studies have yielded sufficient evidence to support an inference that acute exposure to secondhand smoke induces endothelial dysfunction, increases thrombosis, causes inflammation, and potentially affects plaque stability adversely. Those effects appear at concentrations expected to be experienced by people exposed to secondhand smoke.

Data from animal studies also support a dose–response relationship between secondhand-smoke exposure and cardiovascular effects (see Chapter 3 ). The relationship is consistent with the understanding of the pathophysiology of coronary heart disease and the effects of secondhand smoke on humans, including chamber studies. The association comports with known associations between PM, a major constituent of secondhand smoke, and coronary heart disease.

Overall, the pathophysiologic data indicate that it is biologically plausible for secondhand-smoke exposure to have cardiovascular effects, such as effects that lead to cardiovascular disease and acute myocardial infarction (MI). The exact mechanisms by which such effects occur, however, remain to be elucidated.

Smoking-Ban Background

Characteristics of smoking bans can heavily influence their consequences. Interpretation of the results of epidemiologic studies that involve smoking bans must account for information on the bans and their enforcement.

Secondhand smoke should have been measured before and after implementation of a ban, and locations with and without bans should have been compared. Studies that include self-reported assessments of exposure to secondhand smoke cannot necessarily be compared with each other unless the survey instruments (such as interviews) were similar.

The comparability of the time and length of followup of the studies should be assessed. For example, the impact of a ban in one area may differ from the impact of a ban in another solely because the observation times were different and other activities may have occurred during the same periods. In comparing studies, it may be impossible to separate contextual factors associated with ban legislation—such as public comment periods, information announcing the ban, and notices about the impending changes—from the impact of the ban itself. The committee therefore included such contextual factors in drawing conclusions about the effects of a ban.

Interpretation needs to consider the timeframes in the epidemiologic evidence, for example, the time from onset of a smoking ban to the mea-

surement of incidence of a disease, the timing and nature of enforcement, and the time until changes in cardiovascular-event rates were observed in people who had various baseline risks. Interpretation should account for the extent to which studies assessed possible alternative causes of decreases in hospitalizations for coronary events, including changes in health-care availability and in the standard of practice in cardiac care, such as new diagnostic criteria for acute MI during the period of study. The latter is especially important in making before–after comparisons in the absence of a comparison geographic area in which no ban has been implemented.

When designing and analyzing future studies, researchers should examine the time between the implementation of a smoking ban and changes in rates of hospital admission or cardiac death. Future studies could evaluate whether decreases in admissions are transitory, sustained, or increasing, and ideally they would include information on individual subjects, including prior history of cardiac disease, to answer the questions posed to the committee.

Epidemiologic Studies

Cardiovascular disease is a major public-health concern. The results of dozens of epidemiologic studies of both case–control and cohort design carried out in multiple populations consistently indicate about a 25–30% increase in risk of coronary heart disease from exposure to secondhand smoke (see Chapter 4 ). Epidemiologic studies using serum cotinine concentration as a biomarker of overall exposure to secondhand smoke indicated that the relative risk (RR) of coronary heart disease associated with secondhand smoke is even greater than those estimates. The excess risk is unlikely to be explained by misclassification bias, uncontrolled-for confounding effects, or publication bias. Although few studies have addressed the risk of coronary heart disease posed by secondhand-smoke exposure in the workplace, there is no biologically plausible reason to suppose that the effect of secondhand-smoke exposure at work or in a public building differs from the effect of exposure in the home environment. Epidemiologic studies demonstrate a dose–response relationship between chronic secondhand-smoke exposure as assessed by self-reports of exposure (He et al., 1999) and as assessed by biomarkers (cotinine) and long-term risk of coronary heart disease (Whincup et al., 2004). Dose–response curves show a steep initial rise in risk when going from negligible to low exposure followed by a gradual increase with increasing exposure.

The INTERHEART study, a large case–control study of cases of first acute MI, showed that exposure to secondhand smoke increased the risk of nonfatal acute MI in a graded manner (Teo et al., 2006).

Eleven key epidemiologic studies evaluated the effects of eight smok-

ing bans on the incidence of acute coronary events (see Table 8-1 and Chapter 6 ). The results of those studies show remarkable consistency: all showed decreases in the rate of acute MIs after the implementation of smoking bans (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Pell et al., 2008; Sargent et al., 2004; Seo and Torabi, 2007; Vasselli et al., 2008). Two of the studies (Pell et al., 2008; Seo and Torabi, 2007) examined rates of hospitalization for acute coronary events after the implementation of smoking bans and provided direct evidence of the relationship of secondhand-smoke exposure to acute coronary events by presenting results in nonsmokers.

The decreases in acute MIs in the 11 studies ranged from about 6 to 47%, depending on characteristics of the study, including the method of statistical analysis. The consistency in the direction of change gave the committee confidence that smoking bans result in a decrease in the rate of acute MI. The studies took advantage of bans as “natural experiments” to look at questions about the effects of bans, and indirectly of a decrease in secondhand-smoke exposure, on the incidence of acute cardiac events. As discussed in Assessing the Health Impact of Air Quality Regulations: Concepts and Methods for Accountability Research (HEI Accountability Working Group, 2003) in the context of air-pollution regulations, studies of interventions constitute a more definitive approach than other epidemiologic studies to determining whether regulations result in health benefits. All the studies are relevant and informative with respect to the questions posed to the committee, and overall they support an association between smoking bans and a decrease in acute cardiovascular events. The studies have inherent limitations related to their nature, but they directly evaluated the effects of an intervention (a smoking ban, including any concomitant activities) on a health outcome of interest (acute coronary events).

The committee could not determine the magnitude of effect with any reasonable degree of certainty on the basis of those studies. The variability in study design, implementation, and analysis was so large that the committee concluded that it could not conduct a meta-analysis or combine the information from the studies to calculate a point estimate of the effect. In particular, the committee was unable to determine the overall portion of the effect attributable to decreased smoking by smokers as opposed to decreased exposure of nonsmokers to secondhand smoke because of a lack of information on smoking status in nine of the studies (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Seo and Torabi, 2007; Vasselli et al., 2008). The results of the studies are consistent with the findings of the pathophysiologic studies discussed in Chapter 3 and the data on PM discussed in Chapters 3 and 7 . At the population level,

results of the key intervention studies reviewed by the committee are for the most part consistent with a decrease in risk as early as a month following reductions in secondhand-smoke exposure; however, given the variability in the studies and the lack of data on the precise timing of interventions, the smoking-ban studies do not provide adequate information on the time it takes to see decreases in acute MIs.

Plausibility of Effect

The committee considered both the biologic plausibility of a causal relationship between a decrease in secondhand-smoke exposure and a decrease in the incidence of acute MI and the plausibility of the magnitude of the effect seen in the key epidemiologic studies after implementation of smoking bans.

The experimental data reviewed in Chapter 3 demonstrate that several components of secondhand smoke, as well as secondhand smoke itself, exert substantial cardiovascular toxicity. The toxic effects include the induction of endothelial dysfunction, an increase in thrombosis, increased inflammation, and possible reductions in plaque stability. The data provide evidence that it is biologically plausible for secondhand smoke to be a potential causative trigger of acute coronary events. The risk of acute coronary events is likely to be increased if a person has preexisting heart disease. The association comports with findings on air-pollution components, such as diesel exhaust (Mills et al., 2007) and PM (Bhatnagar, 2006).

As a “reality check” on the potential effects of changes in secondhand-smoke exposure, the committee estimated the decrease in risk of cardiovascular disease and specifically heart failure that would be expected on the basis of the risk effects of changes in airborne PM concentrations after implementation of smoking bans seen in the PM literature. The PM in cigarette smoke is not identical with that in air pollution, and the committee did not attempt to estimate the risk attributable to secondhand-smoke exposure through the PM risk estimates but rather found this a useful exercise to see whether the decreases seen in the epidemiologic literature are reasonable, given data on other air pollutants that have some common characteristics. The committee’s estimates on the basis of the PM literature support the possibility that changes in secondhand-smoke exposure after implementation of a smoking ban can have a substantial effect on hospital admissions for heart failure and cardiovascular disease.

SUMMARY OF OVERALL WEIGHT OF EVIDENCE

The committee examined three relationships—of secondhand-smoke exposure and cardiovascular disease, of secondhand-smoke exposure and

TABLE 8-1 Summary of Key Studies (Studies Listed by Smoking-Ban Region in Order of Publication)

acute coronary events, and of smoking bans and acute coronary events. The committee used the criteria of causation described in Smoking and Health: Report of the Advisory Committee of the Surgeon General of the Public Health Service (U.S. Public Health Service, 1964) in drawing conclusions regarding those relationships. The criteria are often referred to as the Bradford Hill criteria because they were, as stated by Hamill (1997), “later expanded and refined by A. B. Hill” (Hill, 1965). Table 8-2 summarizes the available evidence on secondhand-smoke exposure and coronary events in terms of the Bradford Hill criteria.

Secondhand-Smoke Exposure and Cardiovascular Disease

The results of both case–control and cohort studies carried out in multiple populations consistently indicate exposure to secondhand smoke causes about a 25–30% increase in the risk of coronary heart disease; results of some studies indicate a dose–response relationship. Data from animal studies support the dose–response relationship (see Chapter 3 ). Data from experimental studies of animals and cells and from intentional human-dosing studies indicate that a relationship between secondhand-smoke exposure and coronary heart disease is biologically plausible and consistent with understanding of the pathophysiology of coronary heart disease.

Taking all that evidence together, the committee concurs with the conclusions in the 2006 surgeon general’s report (HHS, 2006) that “the evidence is sufficient to infer a causal relationship between exposure to secondhand smoke and increased risks of coronary heart disease morbidity and mortality among both men and women.” Although the committee found strong and consistent evidence of the existence of a positive association between chronic exposure to secondhand smoke and coronary heart disease, determining the magnitude of the risk (the number of cases that are attributable to secondhand-smoke exposure) proved challenging, and the committee has not done it.

Secondhand-Smoke Exposure and Acute Coronary Events

Two of the epidemiologic studies reviewed by the committee that examine rates of hospitalization for acute coronary events after implementation of smoking bans provide direct evidence related to secondhand smoke exposures. The studies either reported events in nonsmokers only (Monroe, Indiana) (Seo and Torabi, 2007) or analyzed nonsmokers and smokers separately on the basis of serum cotinine concentration (Scotland) (Pell et al., 2008). Both studies showed reductions in the RR of acute coronary events in nonsmokers when secondhand-smoke exposure was decreased after implementation of the bans; this indicates an association between a

decrease in exposure to secondhand smoke and a decrease in risk of acute coronary events. Because of differences between and limitations of the two studies (such as in population, population size, and analysis), they do not provide strong sufficient evidence to determine the magnitude of the decrease in RR.

The effect seen after implementation of smoking bans is consistent with data from the INTERHEART study, a case–control study of 15,152 cases of first acute MI in 262 centers in 52 countries (Teo et al., 2006). Increased exposure to secondhand smoke increased the risk of nonfatal acute MI in a graded manner, with adjusted odds ratios of 1.24 (95% confidence interval [CI], 1.17–1.32) and 1.62 (95% CI, 1.45–1.81) in the least exposed people (1–7 hours of exposure per week) and the most exposed (at least 22 hours of exposure per week), respectively. In contrast, a study using data from the Western New York Health Study collected from 1995 to 2001 found that secondhand smoke was not significantly associated with higher risk of MI (Stranges et al., 2007). That study, however, looked at lifetime cumulative exposure to secondhand smoke, a different exposure metric from that in the other studies and one that does not take into account how recent the exposure is.

The other key epidemiologic studies that looked at smoking bans provide indirect evidence of an association between secondhand-smoke exposure and acute coronary events (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Vasselli et al., 2008). Although it is not possible to separate the effect of smoking bans in reducing exposure to secondhand smoke and their effect in reducing active smoking in those studies, because they did not report individual smoking status or secondhand-smoke exposure concentrations, monitoring studies of airborne tracers 1 and biomarkers 2 of exposure to secondhand smoke have demonstrated that exposure to secondhand smoke is dramatically reduced after implementation of smoking bans. Those studies therefore provide indirect evidence that at least part of the decrease in acute coronary events seen after implementation of smoking bans could be mediated by a decrease in exposure to secondhand smoke. It is not possible to determine the differential magnitude of the effect that is attributable to changes in nonsmokers and smokers.

Experimental data show that an association between secondhand-

TABLE 8-2 Evaluation of Available Data in Terms of Bradford-Hill Criteria

smoke exposure and acute coronary events is biologically plausible (see Chapter 3 ). Experimental studies in humans, animals, and cell cultures have demonstrated short-term effects of secondhand smoke as a complex mixture or its components individually (such as oxidants, PM, acrolein, PAHs, benzene, and metals) on the cardiovascular system. There is sufficient evidence from such studies to infer that acute exposure to secondhand smoke at concentrations relevant to population exposures induces endothelial dysfunction, increases inflammation, increases thrombosis, and potentially adversely affects plaque stability. Those effects occur at magnitudes relevant to the pathogenesis of acute coronary events. Furthermore, indirect evidence obtained from studies of ambient PM supports the notion that exposure to PM present in secondhand smoke could trigger acute coronary events or induce arrhythmogenesis in a person with a vulnerable myocardium.

Taking all that evidence together, the committee concludes that there is sufficient evidence of a causal relationship between a decrease in secondhand-smoke exposure and a decrease in the risk of acute MI. Given the variability among studies and their limitations, the committee did not provide a quantitative estimate of the magnitude of the effect.

Smoking Bans and Acute Coronary Events

Nine key studies looked at the overall effect of smoking bans on the incidence of acute coronary events in the overall populations—smokers and nonsmokers—studied (Barone-Adesi et al., 2006; Bartecchi et al., 2006; CDC, 2009; Cesaroni et al., 2008; Juster et al., 2007; Khuder et al., 2007; Lemstra et al., 2008; Sargent et al., 2004; Vasselli et al., 2008). Those studies consistently show a decrease in acute MIs after implementation of smoking bans. The combination of experimental data on secondhand-smoke effects discussed above and exposure data that indicate that secondhand-smoke concentrations decrease substantially after implementation of a smoking ban provides evidence that it is biologically plausible for smoking bans to decrease the rate of acute MIs. The committee concludes that there is an association between smoking bans and a reduction in acute coronary events and, given the temporality and biologic plausibility of the effect, that the evidence is consistent with a causal relationship. Although all the studies demonstrated a positive effect of bans in reducing acute MIs, differences among the studies, including the components of the bans and other interventions that promote smoke-free environments that took place during the bans, limited the committee’s confidence in estimating the overall magnitude of the effect. There is little information on how long it would take for such an effect to be seen inasmuch as the studies have not evaluated periods shorter than a month.

DATA GAPS AND RESEARCH RECOMMENDATIONS

Studies of the effect of indoor smoking bans and secondhand-smoke exposure on acute coronary events should be designed to examine the time between an intervention and changes in the effect and to measure the magnitude of the effect. No time to effect can be postulated for individuals on the basis of the available data, and evaluation of population-based effectiveness of a smoking ban depends on societal actions that implement and enforce the ban and on actions that include smoke reduction in homes, cars, and elsewhere. The decrease in secondhand-smoke exposure does not necessarily occur suddenly—it might decline gradually or by steps. In a likely scenario, once a ban is put into place and enforced, a sharp drop in secondhand-smoke exposure might be seen immediately and followed by a slower decrease in exposure as the population becomes more educated about the health consequences of secondhand smoke and exposure becomes less socially acceptable. Future studies that examine the time from initiation of a ban to observation of an effect and that include followup after initiation of enforcement, taking the social aspects into account, would provide better information on how long it takes to see an effect of a ban. Statistical models should clearly articulate a set of assumptions and include sensitivity analyses. Studies that examine whether decreases in hospital admissions for acute coronary events are transitory or sustained would also be informative.

Many factors are likely to influence the effect of a smoking ban on the incidence and prevalence of acute coronary events in a population. They include age, sex, diet, background risk factors and environmental factors for cardiovascular disease, prevalence of smokers in the community, the underlying rate of heart disease in the community (for example, the rate in Italy versus the United States), and the social environment. Future studies should include direct observations on individuals—including their history of cardiac disease, exposure to other environmental agents, and other risk factors for cardiac events—to assess the impact of those factors on study results. Assessment of smoking status is also needed to distinguish between the effects of secondhand smoke in nonsmokers and the effects of a ban that decreases cigarette consumption or promotes smoking cessation in smokers.

Few constituents of secondhand smoke have been adequately studied for cardiotoxicity. Future research should examine the cardiotoxicity of environmental chemicals, including those in secondhand smoke, to define cardiovascular toxicity end points and establish consistent definitions and measurement standards for cardiotoxicity of environmental contaminants. Specifically, information is lacking on the cardiotoxicity of highly reactive smoke constituents, such as acrolein and other oxidants; on techniques for

quantitating those reactive components; and on the toxicity of low concentrations of benzo[ a ]pyrene, of PAHs other than benzo[a]pyrene, and of mixtures of tobacco-smoke toxicants.

Many questions remain with respect to the pathogenesis of cardiovascular disease and acute coronary events and how secondhand-smoke constituents perturb the pathophysiologic mechanisms and result in disease and death. For example, a better understanding of the factors that promote plaque rupture and how they are influenced by tobacco smoke and PM would provide insight into the mechanisms underlying the cardiovascular effects of secondhand smoke and might lead to better methods of detecting preclinical disease and preventing events.

The committee found only sparse data on the prevalence and incidence of cardiovascular disease and acute coronary events at the national level in general compared with other health end points for which there are central data registries and surveillance of all events, such as the Surveillance, Epidemiology, and End Results (SEER) Program for cancer. Although there are national databases that include acute MI patients—such as the National Registry of Myocardial Infarction (Morrow et al., 2001; Rogers et al., 1994), the Health Care Financing Administration database, and the Cooperative Cardiovascular Project (Ellerbeck et al., 1995)—and the Centers for Disease Control and Prevention’s annual National Hospital Discharge Survey and National Health Interview Survey provide some information on cardiovascular end points, these are not comprehensive or inclusive with respect to hospital participation, patient inclusion, or data capture. A national database that captures all cardiovascular end points would facilitate future epidemiologic studies by allowing the tracking of trends and identification of high-risk populations at a more granular level.

A large prospective cohort study could be very helpful in more accurately estimating the magnitude of the risk of cardiovascular disease and acute coronary events posed by secondhand-smoke exposure. It could be a new study specifically designed to assess effects of secondhand smoke or, as was done with the INTERHEART study, take advantage of existing studies—such as the Framingham Heart Study, the Multi-Ethnic Study of Atherosclerosis, the American Cancer Society’s Cancer Prevention Study-3, the European Prospective Investigation into Cancer and Nutrition study, and the Jackson Heart Study—provided that they have adequate information on individual smoking status and secondhand-smoke exposure (or the ability to measure it, for example, in adequate blood samples). If properly designed, such a study could identify subpopulations at highest risk for acute coronary events from secondhand-smoke exposure in relation to such characteristics as age and sex, and concomitant risk factors, such as obesity.

COMMITTEE RESPONSES TO SPECIFIC QUESTIONS

The committee was tasked with responding to eight specific questions. The questions and the committee’s responses are presented below.

What is the current scientific consensus on the relationship between exposure to secondhand smoke and cardiovascular disease? What is the pathophysiology? What is the strength of the relationship?

On the basis of the available studies of chronic exposure to secondhand smoke and cardiovascular disease, the committee concludes that there is scientific consensus that there is a causal relationship between secondhand-smoke exposure and cardiovascular disease. The results of a number of meta-analyses of the epidemiologic studies showed increases of 25–30% in the risk of cardiovascular disease caused by various exposures. The studies include some that use serum cotinine concentration as a biomarker of exposure and show a dose–response relationship. The pathophysiologic data are consistent with that relationship, as are the data from studies of air pollution and PM. The data in support of the relationship are consistent, but the committee could not calculate a point estimate of the magnitude of the effect (that is, the effect size) given the variable strength of the relationship, differences among studies, poor assessment of secondhand-smoke exposure, and variation in concomitant underlying risk factors.

Is there sufficient evidence to support the plausibility of a causal relation between secondhand smoke exposure and acute coronary events such as acute myocardial infarction and unstable angina? If yes, what is the pathophysiology? And what is the strength of the relationship?

The evidence reviewed by the committee is consistent with a causal relationship between secondhand-smoke exposure and acute coronary events, such as acute MI. It is unknown whether acute exposure, chronic exposure, or a combination of the two underlies the occurrence of acute coronary events, inasmuch as the duration or pattern of exposure in individuals is not known. The evidence includes the results of two key studies that have information on individual smoking status and that showed decreases in risks of acute coronary events in nonsmokers after implementation of a smoking ban. Those studies are supported by information from other smoking-ban studies (although these do not have information on individual smoking status, other exposure-assessment studies have demonstrated that secondhand-smoke exposure decreases after implementation of a smoking ban) and by the large body of literature on PM, especially PM 2.5 , a

constituent of secondhand smoke. The evidence is not yet comprehensive enough to determine a detailed mode of action for the relationship between secondhand-smoke exposure and a variety of intervening and preexisting conditions in predisposing to cardiac events. However, experimental studies have shown effects that are consistent with pathogenic factors in acute coronary events. Although the committee has confidence in the evidence of an association between chronic secondhand-smoke exposure and acute coronary events, the evidence on the magnitude of the association is less convincing, so the committee did not estimate that magnitude (that is, the effect size).

Is it biologically plausible that a relatively brief (e.g., under 1 hour) secondhand smoke exposure incident could precipitate an acute coronary event? If yes, what is known or suspected about how this risk may vary based upon absence or presence (and extent) of preexisting coronary artery disease?

There is no direct evidence that a relatively brief exposure to secondhand smoke can precipitate an acute coronary event; few published studies have addressed that question. The circumstantial evidence of such a relationship, however, is compelling. The strongest evidence comes from airpollution research, especially research on PM. Although the source of the PM can affect its toxicity, particle size in secondhand smoke is comparable with that in air pollution, and research has demonstrated a similarity between cardiovascular effects of PM and of secondhand smoke. Some studies have demonstrated rapid effects of brief secondhand-smoke exposure (for example, on platelet aggregation and endothelial function), but more research is necessary to delineate how secondhand smoke produces cardiovascular effects and the role of underlying preexisting coronary arterial disease in determining susceptibility to the effects. Given the data on PM, especially those from time-series studies, which indicate that a relatively brief exposure can precipitate an acute coronary event, and the fact that PM is a major component of secondhand smoke, the committee concludes that it is biologically plausible for a relatively brief exposure to secondhand smoke to precipitate an acute coronary event.

With respect to how the risk might vary in the presence or absence of preexisting coronary arterial disease, it is generally assumed that acute coronary events are more likely to occur in people who have some level of preexisting disease, although that underlying disease is often subclinical. There are not enough data on the presence of pre-existing coronary arterial disease in the populations studied to assess the extent to which the absence or presence of such preexisting disease affects the cardiovascular risk posed by secondhand-smoke exposure.

What is the strength of the evidence for a causal relationship between indoor smoking bans and decreased risk of acute myocardial infarction?

The key intervention studies that have evaluated the effects of indoor smoking bans consistently have shown a decreased risk of heart attack. Research has also indicated that secondhand-smoke exposure is causally related to heart attacks, that smoking bans decrease secondhand-smoke exposure, and that a relationship between secondhand-smoke exposure and acute coronary events is biologically plausible. All the relevant studies have shown an association in a direction consistent with a causal relationship (although the committee was unable to estimate the magnitude of the association), and the committee therefore concludes that the evidence is sufficient to infer a causal relationship.

What is a reasonable latency period between a decrease in secondhand smoke exposure and a decrease in risk of an acute myocardial infarction for an individual? What is a reasonable latency period between a decrease in population secondhand smoke exposure and a measurable decrease in acute myocardial infarction rates for a population?

No direct information is available on the time between a decrease in secondhand-smoke exposure and a decrease in the risk of a heart attack in an individual. Data on PM, however, have shown effects on the heart within 24 hours, and this supports a period of less than 24 hours. At the population level, results of the key intervention studies reviewed by the committee are for the most part consistent with a decrease in risk as early as a month following reductions in secondhand-smoke exposure; however, given the variability in the studies and the lack of data on the precise timing of interventions, the smoking-ban studies do not provide adequate information on the time it takes to see decreases in heart attacks.

What are the strengths and weaknesses of published population-based studies on the risk of acute myocardial infarction following the institution of comprehensive indoor smoking bans? In light of published studies’ strengths and weaknesses, how much confidence is warranted in reported effect size estimates?

Some of the weaknesses of the published population-based studies of the risk of MI after implementation of smoking bans are

Limitations associated with an open study population and, in some cases, with the use of a small sample.

Concurrent interventions that reduce the observed effect of a smoking ban.

Lack of exposure-assessment criteria and measurements.

Lack of information collected on the time between the cessation of exposure to secondhand smoke and changes in disease rates.

Differences between control and intervention groups.

Nonexperimental design of studies (by necessity).

Lack of assessment of the sensitivity of results to the assumptions made in the statistical analysis.

The different studies had different strengths and weaknesses in relation to the assessment of the effects of smoking bans. For example, the Scottish study had such strengths as prospective design and serum cotinine measurements. The Saskatoon study had the advantage of comprehensive hospital records, and the Monroe County study excluded smokers. The population-based studies of the risk of heart attack after the institution of comprehensive smoking bans were consistent in showing an association between the smoking bans and a decrease in the risk of acute coronary events, and this strengthened the committee’s confidence in the existence of the association. However, because of the weaknesses discussed above and the variability among the studies, the committee has little confidence in the magnitude of the effects and, therefore, thought it inappropriate to attempt to estimate an effect size from such disparate designs and measures.

What factors would be expected to influence the effect size? For example, population age distribution, baseline level of secondhand smoke protection among nonsmokers, and level of secondhand smoke protection provided by the smoke-free law .

A number of factors that vary among the key studies can influence effect size. Although some of the studies found different effects in different age groups, these were not consistently identified. One major factor is the size of the difference in secondhand-smoke exposure before and after implementation of a ban, which would vary and depends on: the magnitude of exposure before the ban, which is influenced by the baseline level of smoking and preexisting smoking bans or restrictions; and the magnitude of exposure after implementation of the ban, which is influenced by the extent of the ban, enforcement of and compliance with the ban, changes in social norms of smoking behaviors, and remaining exposure in areas not covered by the ban (for example, in private vehicles and homes). The baseline rate of acute coronary events or cardiovascular disease could influence the effect

size, as would the prevalence of other risk factors for acute coronary events, such as obesity, diabetes, and age.

What are the most critical research gaps that should be addressed to improve our understanding of the impact of indoor air policies on acute coronary events? What studies should be performed to address these gaps?

The committee identified the following gaps and research needs as those most critical for improving understanding of the effect of indoor-air policies on acute coronary events:

The committee found a relative paucity of data on environmental cardiotoxicity of secondhand smoke compared with other disease end points related to secondhand smoke, such as carcinogenicity and reproductive toxicity. Research should develop standard definitions of cardiotoxic end points in pathophysiologic studies (for example, specific results on standard assays) and a classification system for cardiotoxic agents (similar to the International Agency for Research on Cancer classification of carcinogens). Established cardiotoxicity assays for environmental exposures and consistent definitions of adverse outcomes of such tests would improve investigations of the cardiotoxicity of secondhand smoke and its components and identify potential end points for the investigation of the effects of indoor-air policies on acute coronary events.

The committee found a lack of a system for surveillance of the prevalence of cardiovascular disease and of the incidence of acute coronary events in the United States. Surveillance of incidence and prevalence trends would allow secular trends to be taken into account better and to be compared among different populations to establish the effects of indoor-air policies. Although some national databases and surveys include cardiovascular end points, a national database that tracks hospital admission rates and deaths from acute coronary events, similar to the SEER database for cancer, would improve epidemiologic studies.

The committee found a lack of understanding of a mechanism that leads to plaque rupture and from that to an acute coronary event and of how secondhand smoke affects that process. Additional research is necessary to develop reliable biomarkers of early effects on plaque vulnerability to rupture and to improve the design of pathophysiologic studies of secondhand smoke that examine effects of exposure on plaque stability.

All 11 key studies reviewed by the committee have strengths and limitations due to their study design, and none was designed to test the hypothesis that secondhand-smoke exposure causes cardiovascular disease or acute coronary events. Because of those limitations and the consequent variability in results, the committee did not have enough information to estimate the magnitude of the decrease in cardiovascular risk due to smoking bans or to a decrease in secondhand-smoke exposure. A large, well-designed study could permit estimation of the magnitude of the effect. An ideal study would be prospective; would have individual-level data on smoking status; would account for potential confounders, including other risk factors for cardiovascular events (such as obesity and age), would have biomarkers of mainstream and secondhand-smoke exposures (such as blood cotinine concentrations); and would have enough cases to allow separate analyses of smokers and nonsmokers or, ideally, stratification of cases by cotinine concentrations to examine the dose–response relationship. Such a study could be specifically designed for secondhand smoke or potentially could take advantage of existing cohort studies that might have data available or attainable for investigating secondhand-smoke exposure and its cardiovascular effects, such as was done with the INTERHEART study. Existing studies that could be explored to determine their utility and applicability to questions related to secondhand smoke include the Multi-Ethnic Study of Atherosclerosis (MESA) study, the American Cancer Society’s CPS-3, the European Prospective Investigation of Cancer (EPIC), the Framingham Heart Study, and the Jackson Heart Study. Researchers should clearly articulate the assumptions used in their statistical models and include analysis of the sensitivity of results to model choice and assumptions.

Barone-Adesi, F., L. Vizzini, F. Merletti, and L. Richiardi. 2006. Short-term effects of Italian smoking regulation on rates of hospital admission for acute myocardial infarction. European Heart Journal 27(20):2468-2472.

Bartecchi, C., R. N. Alsever, C. Nevin-Woods, W. M. Thomas, R. O. Estacio, B. B. Bartelson, and M. J. Krantz. 2006. Reduction in the incidence of acute myocardial infarction associated with a citywide smoking ordinance. Circulation 114(14):1490-1496.

Bhatnagar, A. 2006. Environmental cardiology: Studying mechanistic links between pollution and heart disease. Circulation Research 99(7):692-705.

CDC (Centers for Disease Control and Prevention). 2009. Reduced hospitalizations for acute myocardial infarction after implementation of a smoke-free ordinance—city of Pueblo, Colorado, 2002–2006. MMWR—Morbidity & Mortality Weekly Report 57(51):1373-1377.

Cesaroni, G., F. Forastiere, N. Agabiti, P. Valente, P. Zuccaro, and C. A. Perucci. 2008. Effect of the Italian smoking ban on population rates of acute coronary events. Circulation 117(9):1183-1188.

Ellerbeck, E. F., S. F. Jencks, M. J. Radford, T. F. Kresowik, A. S. Craig, J. A. Gold, H. M. Krumholz, and R. A. Vogel. 1995. Quality of care for Medicare patients with acute myocardial infarction. A four-state pilot study from the cooperative cardiovascular project. JAMA 273(19):1509-1514.

Hamill, P. V. 1997. Re: “Invited commentary: Response to Science article, ‘Epidemiology faces its limits.’” American Journal of Epidemiology 146(6):527-528.

He, J., S. Vupputuri, K. Allen, M. R. Prerost, J. Hughes, and P. K. Whelton. 1999. Passive smoking and the risk of coronary heart disease--a meta-analysis of epidemiologic studies. New England Journal of Medicine 340(12):920-926.

HEI (Health Effects Institute) Accountability Working Group. 2003. Assessing the health impact of air quality regulations: Concepts and methods for accountability research. Communication 11. Boston, MA: Health Effects Institute.

HHS (U.S. Department of Health and Human Services). 2006. The health consequences of involuntary exposure to tobacco smoke: A report of the surgeon general. Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, Coordinating Center for Health Promotion, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health.

Hill, A. B. 1965. The environment and disease: Association or causation? Proceedings of the Royal Society of Medicine 58:295-300.

Juster, H. R., B. R. Loomis, T. M. Hinman, M. C. Farrelly, A. Hyland, U. E. Bauer, and G. S. Birkhead. 2007. Declines in hospital admissions for acute myocardial infarction in New York state after implementation of a comprehensive smoking ban. American Journal of Public Health 97(11):2035-2039.

Khuder, S. A., S. Milz, T. Jordan, J. Price, K. Silvestri, and P. Butler. 2007. The impact of a smoking ban on hospital admissions for coronary heart disease. Preventive Medicine 45(1):3-8.

Lemstra, M., C. Neudorf, and J. Opondo. 2008. Implications of a public smoking ban. Canadian Journal of Public Health 99(1):62-65.

Mills, N. L., H. Tornqvist, M. C. Gonzalez, E. Vink, S. D. Robinson, S. Soderberg, N. A. Boon, K. Donaldson, T. Sandstrom, A. Blomberg, and D. E. Newby. 2007. Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease. New England Journal of Medicine 357(11):1075-1082.

Morrow, D. A., E. M. Antman, L. Parsons, J. A. de Lemos, C. P. Cannon, R. P. Giugliano, C. H. McCabe, H. V. Barron, and E. Braunwald. 2001. Application of the TIMI risk score for ST-elevation MI in the National Registry of Myocardial Infarction 3. JAMA 286(11):1356-1359.

Pell, J. P., S. Haw, S. Cobbe, D. E. Newby, A. C. H. Pell, C. Fischbacher, A. McConnachie, S. Pringle, D. Murdoch, F. Dunn, K. Oldroyd, P. Macintyre, B. O’Rourke, and W. Borland. 2008. Smoke-free legislation and hospitalizations for acute coronary syndrome. New England Journal of Medicine 359(5):482-491.

Rogers, W. J., L. J. Bowlby, N. C. Chandra, W. J. French, J. M. Gore, C. T. Lambrew, R. M. Rubison, A. J. Tiefenbrunn, and W. D. Weaver. 1994. Treatment of myocardial infarction in the United States (1990 to 1993). Observations from the National Registry of Myocardial Infarction. Circulation 90(4):2103-2114.

Sargent, R. P., R. M. Shepard, and S. A. Glantz. 2004. Reduced incidence of admissions for myocardial infarction associated with public smoking ban: Before and after study. BMJ 328(7446):977-980.

Seo, D.-C., and M. R. Torabi. 2007. Reduced admissions for acute myocardial infarction associated with a public smoking ban: Matched controlled study. Journal of Drug Education 37(3):217-226.

Stranges, S., M. Cummings, F. P. Cappuccio, and M. Travisan. 2007. Secondhand smoke exposure and cardiovascular disease. Current Cardiovascular Risk Reports 1(5):373-378.

Teo, K. K., S. Ounpuu, S. Hawken, M. R. Pandey, V. Valentin, D. Hunt, R. Diaz, W. Rashed, R. Freeman, L. Jiang, X. Zhang, S. Yusuf, and I. S. Investigators. 2006. Tobacco use and risk of myocardial infarction in 52 countries in the INTERHEART study: A case-control study. Lancet 368(9536):647-658.

U.S. Public Health Service. 1964. Smoking and health: Report of the Advisory Committee of the Surgeon General of the Public Health Service . PHS Publication No. 1103. Washington, DC.

Vasselli, S., P. Papini, D. Gaelone, L. Spizzichino, E. De Campora, R. Gnavi, C. Saitto, N. Binkin, and G. Laurendi. 2008. Reduction incidence of myocardial infarction associated with a national legislative ban on smoking. Minerva Cardioangiologica 56(2):197-203.

Whincup, P. H., J. A. Gilg, J. R. Emberson, M. J. Jarvis, C. Feyerabend, A. Bryant, M. Walker, and D. G. Cook. 2004. Passive smoking and risk of coronary heart disease and stroke: Prospective study with cotinine measurement. BMJ 329(7459):200-205.

Data suggest that exposure to secondhand smoke can result in heart disease in nonsmoking adults. Recently, progress has been made in reducing involuntary exposure to secondhand smoke through legislation banning smoking in workplaces, restaurants, and other public places. The effect of legislation to ban smoking and its effects on the cardiovascular health of nonsmoking adults, however, remains a question.

Secondhand Smoke Exposure and Cardiovascular Effects reviews available scientific literature to assess the relationship between secondhand smoke exposure and acute coronary events. The authors, experts in secondhand smoke exposure and toxicology, clinical cardiology, epidemiology, and statistics, find that there is about a 25 to 30 percent increase in the risk of coronary heart disease from exposure to secondhand smoke. Their findings agree with the 2006 Surgeon General's Report conclusion that there are increased risks of coronary heart disease morbidity and mortality among men and women exposed to secondhand smoke. However, the authors note that the evidence for determining the magnitude of the relationship between chronic secondhand smoke exposure and coronary heart disease is not very strong.

Public health professionals will rely upon Secondhand Smoke Exposure and Cardiovascular Effects for its survey of critical epidemiological studies on the effects of smoking bans and evidence of links between secondhand smoke exposure and cardiovascular events, as well as its findings and recommendations.

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Tobacco, Nicotine, and E-Cigarettes Research Report How can we prevent tobacco use?

Photo of a cigarette that has been put out

The medical consequences of tobacco use—including secondhand exposure—make tobacco control and smoking prevention crucial parts of any public health strategy. Since the first Surgeon General’s Report on Smoking and Health in 1964, states and communities have made efforts to reduce initiation of smoking, decrease exposure to smoke, and increase cessation. Researchers estimate that these tobacco control efforts are associated with averting an estimated 8 million premature deaths and extending the average life expectancy of men by 2.3 years and of women by 1.6 years. 18 But there is a long way yet to go: roughly 5.6 million adolescents under age 18 are expected to die prematurely as a result of an illness related to smoking. 13

Prevention can take the form of policy-level measures, such as increased taxation of tobacco products; stricter laws (and enforcement of laws) regulating who can purchase tobacco products; how and where they can be purchased; where and when they can be used (i.e., smoke-free policies in restaurants, bars, and other public places); and restrictions on advertising and mandatory health warnings on packages. Over 100 studies have shown that higher taxes on cigarettes, for example, produce significant reductions in smoking, especially among youth and lower-income individuals. 217 Smoke-free workplace laws and restrictions on advertising have also shown benefits. 218

Prevention can also take place at the school or community level. Merely educating potential smokers about the health risks has not proven effective. 218 Successful evidence-based interventions aim to reduce or delay initiation of smoking, alcohol use, and illicit drug use, and otherwise improve outcomes for children and teens by reducing or mitigating modifiable risk factors and bolstering protective factors. Risk factors for smoking include having family members or peers who smoke, being in a lower socioeconomic status, living in a neighborhood with high density of tobacco outlets, not participating in team sports, being exposed to smoking in movies, and being sensation-seeking. 219 Although older teens are more likely to smoke than younger teens, the earlier a person starts smoking or using any addictive substance, the more likely they are to develop an addiction. Males are also more likely to take up smoking in adolescence than females.

Some evidence-based interventions show lasting effects on reducing smoking initiation. For instance, communities utilizing the intervention-delivery system, Communities that Care (CTC) for students aged 10 to14 show sustained reduction in male cigarette initiation up to 9 years after the end of the intervention. 220

Persuasive Essay Guide

Persuasive Essay About Smoking

Persuasive Essay About Smoking - Making a Powerful Argument with Examples

What You Need To Know About Persuasive Essay

A persuasive essay is a type of writing that aims to convince its readers to take a certain stance or action. It often uses logical arguments and evidence to back up its argument in order to persuade readers.

It also utilizes rhetorical techniques such as ethos, pathos, and logos to make the argument more convincing. In other words, persuasive essays use facts and evidence as well as emotion to make their points.

A persuasive essay about smoking would use these techniques to convince its readers about any point about smoking. Check out an example below:

Simple persuasive essay about smoking

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Persuasive Essay Examples About Smoking

Smoking is one of the leading causes of preventable death in the world. It leads to adverse health effects, including lung cancer, heart disease, and damage to the respiratory tract. However, the number of people who smoke cigarettes has been on the rise globally.

A lot has been written on topics related to the effects of smoking. Reading essays about it can help you get an idea of what makes a good persuasive essay.

Here are some sample persuasive essays about smoking that you can use as inspiration for your own writing:

Persuasive speech on smoking outline

Persuasive essay about smoking should be banned

Persuasive essay about smoking pdf

Persuasive essay about smoking cannot relieve stress

Persuasive essay about smoking in public places

Speech about smoking is dangerous

Persuasive Essay About Smoking Introduction

Persuasive Essay About Stop Smoking

Short Persuasive Essay About Smoking

Stop Smoking Persuasive Speech

Check out some more persuasive essay examples on various other topics.

Argumentative Essay About Smoking Examples

An argumentative essay is a type of essay that uses facts and logical arguments to back up a point. It is similar to a persuasive essay but differs in that it utilizes more evidence than emotion.

If you’re looking to write an argumentative essay about smoking, here are some examples to get you started on the arguments of why you should not smoke.

Argumentative essay about smoking pdf

Argumentative essay about smoking in public places

Argumentative essay about smoking introduction

Check out the video below to find useful arguments against smoking:

Tips for Writing a Persuasive Essay About Smoking

You have read some examples of persuasive and argumentative essays about smoking. Now here are some tips that will help you craft a powerful essay on this topic.

Choose a Specific Angle

Select a particular perspective on the issue that you can use to form your argument. When talking about smoking, you can focus on any aspect such as the health risks, economic costs, or environmental impact.

Think about how you want to approach the topic. For instance, you could write about why smoking should be banned.

Check out the list of persuasive essay topics to help you while you are thinking of an angle to choose!

Research the Facts

Before writing your essay, make sure to research the facts about smoking. This will give you reliable information to use in your arguments and evidence for why people should avoid smoking.

You can find and use credible data and information from reputable sources such as government websites, health organizations, and scientific studies.

For instance, you should gather facts about health issues and negative effects of tobacco if arguing against smoking. Moreover, you should use and cite sources carefully.

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Make an Outline

The next step is to create an outline for your essay. This will help you organize your thoughts and make sure that all the points in your essay flow together logically.

Your outline should include the introduction, body paragraphs, and conclusion. This will help ensure that your essay has a clear structure and argument.

Use Persuasive Language

When writing your essay, make sure to use persuasive language such as “it is necessary” or “people must be aware”. This will help you convey your message more effectively and emphasize the importance of your point.

Also, don’t forget to use rhetorical devices such as ethos, pathos, and logos to make your arguments more convincing. That is, you should incorporate emotion, personal experience, and logic into your arguments.

Introduce Opposing Arguments

Another important tip when writing a persuasive essay on smoking is to introduce opposing arguments. It will show that you are aware of the counterarguments and can provide evidence to refute them. This will help you strengthen your argument.

By doing this, your essay will come off as more balanced and objective, making it more convincing.

Finish Strong

Finally, make sure to finish your essay with a powerful conclusion. This will help you leave a lasting impression on your readers and reinforce the main points of your argument. You can end by summarizing the key points or giving some advice to the reader.

A powerful conclusion could either include food for thought or a call to action. So be sure to use persuasive language and make your conclusion strong.

To conclude,

By following these tips, you can write an effective and persuasive essay on smoking. Remember to research the facts, make an outline, and use persuasive language.

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How To Write A Smoking Essay That Will Blow Your Classmates out of the Water

Writing a Smoking Essay. Complete Actionable Guide

A smoking essay might not be your first choice, but it is a common enough topic, whether it is assigned by a professor or left to your choice. Today we’ll take you through the paces of creating a compelling piece, share fresh ideas for writing teen smoking essays, and tackle the specifics of the essential parts of any paper, including an introduction and a conclusion.

Why Choose a Smoking Essay?

If you are free to select any topic, why would you open this can of worms? There are several compelling arguments in favor, such as:

A smoking essay can fit any type of writing assignment. You can craft an argumentative essay about smoking, a persuasive piece, or even a narration about someone’s struggle with quitting. It’s a rare case of a one-size-fits-all topic.
There is an endless number of environmental essay topics ideas . From the reasons and history of smoking to health and economic impact, as well as psychological and physiological factors that make quitting so challenging.
A staggering number of reliable sources are available online. You won’t have to dig deep to find medical or economic research, there are thousands of papers published in peer-reviewed journals, ready and waiting for you to use them.

Essential Considerations for Your Essay on Smoking

Whether you are writing a teenage smoking essay or a study of health-related issues, you need to stay objective and avoid including any judgment into your assignment. Even if you are firmly against smoking, do not let emotions direct your writing. You should also keep your language tolerant and free of offensive remarks or generalizations.

The rule of thumb is to keep your piece academic. It is an essay about smoking cigarettes you have to submit to your professor, not a blog post to share with friends.

How to Generate Endless Smoking Essay Topic Ideas

At first, it might seem that every theme has been covered by countless generations of your predecessors. However, there are ways to add a new spin to the dullest of topics. We’ll share a unique approach to generating new ideas and take the teenage smoking essay as an example. To make it fresh and exciting, you can:

Add a historic twist to your topic. For instance, research the teenage smoking statistics through the years and theorize the factors that influence the numbers.
Compare the data across the globe. You can select the best scale for your paper, comparing smoking rates in the neighboring cities, states, or countries.
Look at the question from an unexpected perspective. For instance, research how the adoption of social media influenced smoking or whether music preferences can be related to this habit.

The latter approach on our list will generate endless ideas for writing teen smoking essays. Select the one that fits your interests or is the easiest to research, depending on the time and effort you are willing to put into essay writing .

How To Write An Essay About Smoking Cigarettes

A smoking essay follows the same rules as an academic paper on any other topic. You start with an introduction, fill the body paragraphs with individual points, and wrap up using a conclusion. The filling of your “essay sandwich” will depend on the topic, but we can tell for sure what your opening and closing paragraphs should be like.

Smoking Essay Introduction

Whether you are working on an argumentative essay about smoking or a persuasive paper, your introduction is nothing but a vessel for a thesis statement. It is the core of your essay, and its absence is the first strike against you. Properly constructed thesis sums up your point of view on the economic research topics and lists the critical points you are about to highlight. If you allude to the opposing views in your thesis statement, the professor is sure to add extra points to your grade.

The first sentence is crucial for your essay, as it sets the tone and makes the first impression. Make it surprising, exciting, powerful with facts, statistics, or vivid images, and it will become a hook to lure the reader in deeper.

Round up the introduction with a transition to your first body passage and the point it will make. Otherwise, your essay might seem disjointed and patchy. Alternatively, you can use the first couple of sentences of the body paragraph as a transition.

Smoking Essay Conclusion

Any argumentative and persuasive essay on smoking must include a short conclusion. In the final passage, return to your thesis statement and repeat it in other words, highlighting the points you have made throughout the body paragraphs. You can also add final thoughts or even a personal opinion at the end to round up your assignment.

Think of the conclusion as a mirror reflection of your introduction. Start with a transition from the last body paragraph, follow it with a retelling of your thesis statement, and complete the passage with a powerful parting thought that will stay with the reader. After all, everyone remembers the first and last points most vividly, and your opening and closing sentences are likely to have a significant influence on the final grade.

Bonus Tips on How to Write a Persuasive Essay About Smoking

With the most challenging parts of the smoking essay out of the way, here are a couple of parting tips to ensure your paper gets the highest grade possible:

Do not rely on samples you find online to guide your writing. You can never tell what grade a random essay about smoking cigarettes received. Unless you use winning submissions from essay competitions, you might copy faulty techniques and data into your paper and get a reduced grade.
Do not forget to include references after the conclusion and cite the sources throughout the paper. Otherwise, you might get accused of academic dishonesty and ruin your academic record. Ask your professor about the appropriate citation style if you are not sure whether you should use APA, MLA, or Chicago.
Do not submit your smoking essay without editing and proofreading first. The best thing you can do is leave the piece alone for a day or two and come back to it with fresh eyes and mind to check for redundancies, illogical argumentation, and irrelevant examples. Professional editing software, such as Grammarly, will help with most typos and glaring errors. Still, it is up to you to go through the paper a couple of times before submission to ensure it is as close to perfection as it can get.
Do not be shy about getting help with writing smoking essays if you are out of time. Professional writers can take over any step of the writing process, from generating ideas to the final round of proofreading. Contact our agents or skip straight to the order form if you need our help to complete this assignment.

We hope our advice and ideas for writing teen smoking essays help you get out of the slump and produce a flawless piece of writing worthy of an A. For extra assistance with choosing the topic, outlining, writing, and editing, reach out to our support managers .

Essay on Smoking

500 words essay on smoking.

One of the most common problems we are facing in today’s world which is killing people is smoking. A lot of people pick up this habit because of stress , personal issues and more. In fact, some even begin showing it off. When someone smokes a cigarette, they not only hurt themselves but everyone around them. It has many ill-effects on the human body which we will go through in the essay on smoking.

Ill-Effects of Smoking

Tobacco can have a disastrous impact on our health. Nonetheless, people consume it daily for a long period of time till it’s too late. Nearly one billion people in the whole world smoke. It is a shocking figure as that 1 billion puts millions of people at risk along with themselves.

Cigarettes have a major impact on the lungs. Around a third of all cancer cases happen due to smoking. For instance, it can affect breathing and causes shortness of breath and coughing. Further, it also increases the risk of respiratory tract infection which ultimately reduces the quality of life.

In addition to these serious health consequences, smoking impacts the well-being of a person as well. It alters the sense of smell and taste. Further, it also reduces the ability to perform physical exercises.

It also hampers your physical appearances like giving yellow teeth and aged skin. You also get a greater risk of depression or anxiety . Smoking also affects our relationship with our family, friends and colleagues.

Most importantly, it is also an expensive habit. In other words, it entails heavy financial costs. Even though some people don’t have money to get by, they waste it on cigarettes because of their addiction.

How to Quit Smoking?

There are many ways through which one can quit smoking. The first one is preparing for the day when you will quit. It is not easy to quit a habit abruptly, so set a date to give yourself time to prepare mentally.

Further, you can also use NRTs for your nicotine dependence. They can reduce your craving and withdrawal symptoms. NRTs like skin patches, chewing gums, lozenges, nasal spray and inhalers can help greatly.

Moreover, you can also consider non-nicotine medications. They require a prescription so it is essential to talk to your doctor to get access to it. Most importantly, seek behavioural support. To tackle your dependence on nicotine, it is essential to get counselling services, self-materials or more to get through this phase.

One can also try alternative therapies if they want to try them. There is no harm in trying as long as you are determined to quit smoking. For instance, filters, smoking deterrents, e-cigarettes, acupuncture, cold laser therapy, yoga and more can work for some people.

Always remember that you cannot quit smoking instantly as it will be bad for you as well. Try cutting down on it and then slowly and steadily give it up altogether.

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

Conclusion of the Essay on Smoking

Thus, if anyone is a slave to cigarettes, it is essential for them to understand that it is never too late to stop smoking. With the help and a good action plan, anyone can quit it for good. Moreover, the benefits will be evident within a few days of quitting.

FAQ of Essay on Smoking

Question 1: What are the effects of smoking?

Answer 1: Smoking has major effects like cancer, heart disease, stroke, lung diseases, diabetes, and more. It also increases the risk for tuberculosis, certain eye diseases, and problems with the immune system .

Question 2: Why should we avoid smoking?

Answer 2: We must avoid smoking as it can lengthen your life expectancy. Moreover, by not smoking, you decrease your risk of disease which includes lung cancer, throat cancer, heart disease, high blood pressure, and more.

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Home — Essay Samples — Nursing & Health — Addictions — Smoking

Essays About Smoking

Smoking essay, types of essay about smoking.

Cause and Effect Essay: This type of essay focuses on the causes and effects of smoking. It discusses why people start smoking and the consequences of smoking on both the smoker and those around them.
Argumentative Essay: This essay type aims to persuade the reader about the negative effects of smoking. It presents an argument and provides supporting evidence to convince the reader that smoking is harmful and should be avoided.
Persuasive Essay: Similar to an argumentative essay, this type of essay aims to persuade the reader to quit smoking. It presents facts, statistics, and other relevant information to convince the reader to stop smoking.

Smoking Essay Example: Cause and Effect

Identify the causes of smoking: Start by examining why people start smoking in the first place. Is it peer pressure, addiction, stress, or curiosity? Understanding the reasons why people smoke is crucial in creating an effective cause and effect essay.
Discuss the effects of smoking: Highlight the impact smoking has on an individual's health and the environment. Discuss the risks associated with smoking, such as lung cancer, heart disease, and respiratory problems, and explain how smoking affects non-smokers through secondhand smoke.
Use reliable sources: To make your essay more convincing, ensure that you use credible sources to back up your claims. Use scientific studies, government reports, and medical journals to support your arguments.
Provide statistical evidence: Incorporate statistical data to make your essay more impactful. Use figures to show the number of people who smoke, the effects of smoking on the environment, and the costs associated with smoking.
Offer solutions: Conclude your essay by suggesting solutions to the problem of smoking. Encourage smokers to quit by outlining the benefits of quitting smoking and offering resources for those who want to quit.

Smoking: Argumentative Essay

Choose a clear position: The writer should choose a side on the issue of smoking, either for or against it, and be clear in presenting their stance.
Gather evidence: Research and collect facts and statistics to support the writer's argument. They can find data from reliable sources like scientific journals, government reports, and reputable news organizations.
Address counterarguments: A good argumentative essay will acknowledge opposing viewpoints and then provide a counterargument to refute them.
Use persuasive language: The writer should use persuasive language to convince the reader of their position. This includes using rhetorical devices, such as ethos, pathos, and logos, to appeal to the reader's emotions and logic.
Provide a clear conclusion: The writer should summarize the key points of their argument and reiterate their stance in the conclusion.

Persuasive Essay on Smoking

Identify your audience and their beliefs about smoking.
Present compelling evidence to support your argument, such as statistics, research studies, and personal anecdotes.
Use emotional appeals, such as stories or images that show the negative impact of smoking.
Address potential counterarguments and refute them effectively.
Use strong and clear language to persuade the reader to take action.
When choosing a topic for a smoking persuasive essay, consider a specific aspect of smoking that you would like to persuade the audience to act upon.

Hook Examples for Smoking Essays

Anecdotal hook.

Imagine a teenager taking their first puff of a cigarette, unaware of the lifelong addiction they're about to face. This scenario illustrates the pervasive issue of smoking among young people.

Question Hook

Is the pleasure derived from smoking worth the serious health risks it poses? Dive into the contentious debate over tobacco use and its consequences.

Quotation Hook

"Smoking is a habit that drains your money and kills you slowly, one puff after another." — Unknown. Explore the financial and health impacts of smoking in today's society.

Statistical or Factual Hook

Did you know that smoking is responsible for nearly 8 million deaths worldwide each year? Examine the alarming statistics and data associated with tobacco-related illnesses.

Definition Hook

What exactly is smoking, and what are the various forms it takes? Delve into the definitions of smoking, including cigarettes, cigars, pipes, and emerging alternatives like e-cigarettes.

Rhetorical Question Hook

Can we truly call ourselves a smoke-free generation when new nicotine delivery devices are enticing young people? Investigate the impact of vaping and e-cigarettes on the youth.

Historical Hook

Trace the history of smoking, from its ancient roots to its prevalence in different cultures and societies. Explore how perceptions of smoking have evolved over time.

Contrast Hook

Contrast the images of the suave, cigarette-smoking characters from classic films with the grim reality of tobacco-related diseases and addiction in the modern world.

Narrative Hook

Walk in the shoes of a lifelong smoker as they recount their journey from that first cigarette to a battle with addiction and the quest to quit. Their story reflects the struggles of many.

Shocking Statement Hook

Prepare to uncover the disturbing truth about smoking—how it not only harms the smoker but also affects non-smokers through secondhand smoke exposure. It's an issue that goes beyond personal choice.

Smoking Informative Speech

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Rhetorical Analysis of Anti-smoking Campaigns

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The History of Tobacco Use and Its Dangers

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How Smoking Can Ruin Your Health

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Smoking: Causes and Effects Essay

Among numerous bad habits of modern society smoking seems to be of the greatest importance. Not only does it affect the person who smokes, but also those who are around him. Many people argue about the appropriate definition of smoking, whether it is a disease or just a bad habit. Considering the peculiarities of a habit and of a disease, smoking can be considered as a habit rather than a disease. Among signifiers of a bad habit, it should be pointed out that a bad habit can be controlled by willpower, it can be prevented, and it can be cured (Gilman and Zun 33). Smoking can be fought against with the help of all the points mentioned above. Thus, it is a bad habit which can be easily refused if an individual possessing it has a strong decision to quit. Moreover, it can be cured in many different ways, and it can be prevented by education and other social norms.

Considering the first element, which one of the most important out of the three, willpower is a key to get rid of such a bad habit as smoking, which is very difficult to give up. If a person has a strong determination to quit smoking, he will have to endure considerably a short period of time of physical discomfort. One of the most important part of quitting, is that that is doesn’t require medical help, that is to say, a person is not likely to suffer a procedure that is risky to health and life. In comparison to alcoholism or drug addiction, where medical help is essential to save life of a person who needs a certain amount of an alcohol or drug substance in has blood to survive, the lack of nicotine in blood produces just a physical discomfort that is not dangerous for health and can be handled with the help of willpower. Regarding the second aspect of a bad habit, prevention, smoking can be prevented in early childhood with the help of proper education and social norms (Brinkman et al 689). Many people start smoking when they are teenagers just to prove they are adults in companies. If the society was able to produce a negative impression of this bad habit, so that it doesn’t seem to be sign of being an adult, it would be easier to prevent many children from smoking (Albaum et al 11).

The last aspect of a bad habit is a cure for it. Smoking can be cured in many different ways. There are many different techniques, starting from a nicotine plaster and ending with special clinics and communities helping people to get rid of this problem. If a person wants to quit, he or she has various options to help him or her to solve this problem. To conclude, smoking is a bad habit that can be easily quitted. Although there is an addiction to smoking, the lack of nicotine is not dangerous to the life of a smoker and can be handled without medical intervention. The most important aspect of this bad habit, which actually makes a habit, is that it can be quitted with the help of willpower. Moreover, it can be prevented with alteration of attitude towards smoking and it can be cured in many different ways (Albaum et al 23).

Despite widespread public awareness of the multiple health risks associated with smoking, one out of every four girls under age 18 is a smoker and more than 25 million American women smoke. Whereas the last two decades have seen an overall decrease in smoking prevalence, the rate of smoking has declined much more slowly among women than among men. If current trends continue, smoking rates of women will overtake those of men by the year 2000. Smoking rates are highest, approaching 30%, among women of reproductive age (18–44 years). Rates of smoking are particularly high among young White women with a high school education or less and low income. Cessation rates are lower among African American women (30% have quit) compared to White women (43% have quit). Minority and young women who have low rates of self-initiated cessation are also underrepresented in formal smoking cessation programs (Gilman and Zun 87). A greater proportion of women than men are pre-contemplators, that is, not considering quitting smoking within 6 months and have lower self-confidence that they could quit if they were to try. The debate continues regarding whether or not women are less likely to be successful at quitting when they try than men, with some evidence suggesting that women are more likely than men to relapse and others indicating no gender differences). Regardless, rates of relapse are very high, both among self-quitters and those who participate in formal cessation programs (Albaum et al 24).

Interventions specifically designed for smokers have attempted to address the role of weight concerns as an inhibitor to cessation and long-term maintenance. A randomized trial tested nicotine gum or a behavioral weight control program each alone, or in combination as adjuncts to an intensive group cessation intervention for weight concerned women smokers. The intervention integrated accepted cognitive and behavioral coping strategies for quitting smoking, changing eating behaviors, and developing a walking program.

Works Cited

Albaum, G., Baker, K.G., Hozier, G.C., Rogers, R.D. Smoking Behavior, Information Sources, and Consumption Values of Teenagers: Implications for Public Policy and Other Intervention Failures. Journal of Consumer Affairs , 36 (1), 2002: 5-55.

Brinkman, M.C., Callahan, P.J., Gordon, S.M., Kenny, D.V., Wallace, L.A. Volatile Organic Compounds as Breath Biomarkers for Active and Passive Smoking. Environmental Health Perspectives, 110 (7), 2002, p. 689.

Gilman Sander L. and Xhou Zun. Smoke: A GlobalHistory of Smoking. Reaktion Books; illustrated edition edition, 2004.

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IvyPanda. (2021, November 29). Smoking: Causes and Effects. https://ivypanda.com/essays/smoking-causes-and-effects/

"Smoking: Causes and Effects." IvyPanda , 29 Nov. 2021, ivypanda.com/essays/smoking-causes-and-effects/.

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IvyPanda . 2021. "Smoking: Causes and Effects." November 29, 2021. https://ivypanda.com/essays/smoking-causes-and-effects/.

1. IvyPanda . "Smoking: Causes and Effects." November 29, 2021. https://ivypanda.com/essays/smoking-causes-and-effects/.

Bibliography

IvyPanda . "Smoking: Causes and Effects." November 29, 2021. https://ivypanda.com/essays/smoking-causes-and-effects/.

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Smoking Patients. Practice Recommendations

Evidence for practice recommendations, application of practice recommendation, reflection on the three practice recommendations.

There are several ways to handle smoking patients. 1.1 work recommendation relating to integrating tobacco management into daily practice suggests “brief interventions to screen all clients for all forms of tobacco use and initiate treatment as appropriate” (RNAO, 2017). This nursing necessity fits in Mr. Philobosan’s case because he has just realized that his cigarette use has led him to chronic obstructive pulmonary disease (COPD). Mr Philobosan wishes he could stop smoking, and the health care provider has to assess to understand whether Mr. Philobosan wants to change or is scared of the present situation.

The second strategy, as per 2.1 working manual notes, is to “develop a person-centered tobacco intervention plan with the client” (RNAO, 2017). This medical requirement is applicable in Mr. Philobosan’s case because he has used tobacco for the better part of his life. For a nurse to get any good results with this client, treatment has to focus on unique features to Mr. Philobosan concerning smoking.

Thirdly, section 3.1 recommendation says that it is necessary to “provide clients with, refer them to, intensive interventions and counseling on the use of pharmacotherapy, and express an interest in reducing or quitting tobacco use” (RNAO, 2017). This section is relevant to the client because he has smoked for more than half of his life. The aforementioned means that tobacco is part of Mr. Philobosan’s living, and quitting will not be an easy task as it will require serious treatment, and medical and psychological intervention.

Evidence to support practice recommendation 1.1 argues that brief treatment can raise the probability of an effective quit trial. The initial intercession further increases the time a patient remains free from tobacco after starting their medication. The short-term therapy has the possibility of leading to long-term healing goals (RNAO, 2017). Moreover, the evidence shows that smoking termination therapy offered by clinicians who have the first conduct with the patient are efficient in helping individuals quit smoking.

Working sanction 2.1 indicates that each client is unique and comes with special needs and characteristics which should be looked at for effective service delivery. The personal aspects might be physical, emotional, psychological, cultural or socio-economical, influencing individual lifestyles (RNAO, 2017). Additionally, the therapist should be aware of their biases which can hinder the client’s healing process and focus mainly on what benefits the patient. The medics and their customers should collaborate to pinpoint obstacles to stopping client-specific tobacco use.

Information to validate nursing guideline 3.1 suggests that intensive interventions are a phase to evaluate the inspiration behind the need for the client to stop using tobacco. This practice also incorporates categorization of risky circumstances, triggers to smoke, and discussion of problem-solving tactics to control the hazardous environments. Exhaustive therapy contains behavioral management and counseling, nicotine replacement therapy and prescription medicine (RNAO, 2017). It is recommended that if the clinician is not able to offer thorough treatment, he or she should refer the patient to where they can get the resources.

In the case scenario, Mr. Philobosan has developed chronic obstructive pulmonary disease and is suspected of having a lung infection from smoking tobacco. Using nursing guideline 1.1 as a nurse taking care of him, I will do a thorough screening on his tobacco use history. I will then proceed with brief interventions and inform Mr. Philobosan how tobacco has damaged his lungs leading to infection and his current condition of inability to breathe normally. Further, I will request him not to use tobacco while admitted to the hospital. I will be concurrently medicating for the withdrawal symptoms if Mr. Philobosan exhibits any.

The 2.1 clinical guidelines in integrating tobacco interventions in daily practice will help me explore with the client and develop a unique rehabilitation plan for Mr. Philobosan. First, I would assess how and why he began using nicotine. Secondly, I could investigate what has encouraged his behavior for so many years. Thirdly, I might ask to what extent he thinks he can quit his fifty-year lifestyle. Lastly, I can enquire to understand how he thinks he can end smoking. With the above information, I will develop a client-centered model which considers client characteristics which can impact healing and those which can trigger a relapse.

After developing the client-centered approach plan, 3.1 clinical sanctions will guide me in begging intensive interventions for Mr. Philobosam. In this stage, I can engage both counseling and medication. I will take the client through the first therapeutic session and explain the exact condition he is in currently. The following sessions will deal with factors that have influenced the client’s behavior in the past and aspects that could hinder the healing process. The psychological treatment will be done together with relevant medication. This will commence if my client is ready and willing to change.

From the three best practice guidelines used in this case study, I have learned that most patients do not fully realize the magnitude of their illnesses or conditions until it is elaborated by a professional. As a medic, I have understood that it is our duty to support these clients and guide them systematically through the healing process. One important thing I have learned is that every person whom we serve is unique, and treatment should be client-centered. I have captured that it is essential to work together with the patient to achieve maximum recovery.

RNAO. (2017). Integrating Tobacco interventions into daily practice . Registered Nurses’ Association of Ontario.

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Bibliography

StudyCorgi . "Smoking Patients. Practice Recommendations." September 7, 2022. https://studycorgi.com/smoking-patients-practice-recommendations/.

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About Health Effects of Cigarette Smoking
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Health Effects of Cigarettes: Reproductive Health

At a glance.

Smoking before or during pregnancy can cause serious health problems for the pregnant person and their baby.
Secondhand smoke exposure is harmful during pregnancy and after the baby is born.
Smoking can cause fertility problems for people trying to become pregnant.
Quitting smoking at any time during pregnancy can help protect a pregnant person's health and give babies a healthier start on life.

Pregnant woman lying on sofa at home looking at the ultrasound scan photo of her baby

Smoking and pregnancy

Smoking before or during pregnancy can cause serious problems. Smoking can cause pregnancy complications. It can also harm the health of the pregnant person and their baby. 1 2 Complications and harms include: 3 4 5

Pregnancy complications. Smoking doubles the risk of abnormal bleeding during pregnancy and delivery. This is dangerous for the pregnant person and baby. Other complications include the premature rupture of membranes, placenta previa, placental abruption, and ectopic pregnancy.
Stillbirth. Pregnant people who smoke are at greater risk of stillbirth. Stillbirth is the loss of a baby after the 20th week of pregnancy or during birth.
Poor fetal growth and low birth weight. Smoking slows a baby's growth before birth. Pregnant people who smoke may deliver a baby that is too small, even after a full-term pregnancy.
Premature or preterm delivery. Pregnant people who smoke may deliver a baby early, before 37 weeks of pregnancy. Premature babies often have health problems.
Damage to a baby's developing lungs and brain. Smoking can cause damage that can last through childhood and into the teen years.
Raising the risk for birth defects. Birth defects include cleft lip, cleft palate, or both. A cleft is an opening in a baby's lip or in the roof of the mouth (palate). A baby with a cleft lip can have trouble eating. The baby will likely need surgery to repair the cleft.
Sudden infant death syndrome (SIDS). Smoking increases the risk for SIDS, the 'sudden and unexplained' death of a baby.

Smoking and fertility

Smoking can cause fertility problems . Smoking can make it more difficult for women to get pregnant and increases the risk of never becoming pregnant. 3 4

Smoking also damage sperm. It can also lead to impotence (erectile dysfunction, or ED). Both problems can make it harder to father a baby. 1 2

Secondhand smoke exposure and pregnancy

Secondhand smoke exposure is harmful during pregnancy and after the baby is born. 3

Secondhand smoke exposure during pregnancy causes lower birth weight. It may also cause preterm delivery.
Babies exposed to secondhand smoke are at higher risk for SIDS. They are also at risk for ear infections, lung infections, and decreased lung function.

Quitting smoking can benefit pregnant people and their babies

Quitting smoking is important to have a healthy pregnancy and a healthy baby. The best time to quit smoking is before you try to get pregnant. The next best time to quit is as early in pregnancy as possible. But quitting at any time during pregnancy is helpful. It can help protect a pregnant person's health and give babies a healthier start on life. 5

Quitting smoking: 5

During pregnancy reduces the effects of smoking on the baby's growth.
Before or during early pregnancy reduces the risk for a small or lower birth weight baby.
May also reduce the risk of premature or preterm delivery and early menopause.

Protect your baby by quitting smoking. You can quit. For free help: 1-800-QUIT-NOW. CDC.gov/quit.

Continue reading

CDC.gov/quit
Substance Use During Pregnancy
Smoking, Pregnancy, and Babies
E-Cigarettes and Pregnancy
Maternal and Infant Health
Tobacco Use and Cessation Resources Healthcare Providers
U.S. Department of Health and Human Services. How Tobacco Smoke Causes Disease: The Biology and Behavioral Basis for Smoking-Attributable Disease A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Accessed: April 24, 2024. https://www.ncbi.nlm.nih.gov/books/NBK53017/
U.S. Department of Health and Human Services. The Health Consequences of Smoking—50 Years of Progress: A Report of the Surgeon General. Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2014. Accessed: April 24, 2024. https://www.ncbi.nlm.nih.gov/books/NBK179276/pdf/Bookshelf_NBK179276.pdf
U.S. Department of Health and Human Services. A Report of the Surgeon General: Highlights: Overview of Finding Regarding Reproductive Health . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2010. Accessed: April 24, 2024. https://www.cdc.gov/tobacco/data_statistics/sgr/2010/highlight_sheets/pdfs/overview_reproductive.pdf
U.S. Department of Health and Human Services. The Health Consequences of Smoking: What It Means to You . Atlanta: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2004. Accessed: April 24, 2024. https://www.cdc.gov/tobacco/sgr/2004/index.htm
U.S. Department of Health and Human Services. Smoking Cessation: A Report of the Surgeon General . Atlanta, GA: U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Office on Smoking and Health, 2020. Accessed: April 24, 2024. https://www.hhs.gov/sites/default/files/2020-cessation-sgr-full-report.pdf

Smoking and Tobacco Use

Commercial tobacco use is the leading cause of preventable disease, disability, and death in the United States.

For Everyone

Health care providers, public health.

Two decades of studies suggest health benefits associated with plant-based diets

But researchers caution against broad diet recommendations until remaining knowledge gaps are filled.

Vegetarian and vegan diets are generally associated with better status on various medical factors linked to cardiovascular health and cancer risk, as well as lower risk of cardiovascular diseases, cancer, and death, according to a new review of 49 previously published papers. Angelo Capodici and colleagues present these findings in the open-access journal PLOS ONE on May 15, 2024.

Prior studies have linked certain diets with increased risk of cardiovascular disease and cancer. A diet that is poor in plant products and rich in meat, refined grains, sugar, and salt is associated with higher risk of death. Reducing consumption of animal-based products in favor of plant-based products has been suggested to lower the risk of cardiovascular disease and cancer. However, the overall benefits of such diets remain unclear.

To deepen understanding of the potential benefits of plant-based diets, Capodici and colleagues reviewed 48 papers published between January 2000 and June 2023 that themselves compiled evidence from multiple prior studies. Following an "umbrella" review approach, they extracted and analyzed data from the 48 papers on links between plant-based diets, cardiovascular health, and cancer risk.

Their analysis showed that, overall, vegetarian and vegan diets have a robust statistical association with better health status on a number of risk factors associated with cardiometabolic diseases, cancer, and mortality, such as blood pressure, management of blood sugar, and body mass index. Such diets are associated with reduced risk of ischemic heart disease, gastrointestinal and prostate cancer, and death from cardiovascular disease.

However, among pregnant women specifically, those with vegetarian diets faced no difference in their risk of gestational diabetes and hypertension compared to those on non-plant-based diets.

Overall, these findings suggest that plant-based diets are associated with significant health benefits. However, the researchers note, the statistical strength of this association is significantly limited by the many differences between past studies in terms of the specific diet regimens followed, patient demographics, study duration, and other factors. Moreover, some plant-based diets may introduce vitamin and mineral deficiencies for some people. Thus, the researchers caution against large-scale recommendation of plant-based diets until more research is completed.

The authors add: "Our study evaluates the different impacts of animal-free diets for cardiovascular health and cancer risk showing how a vegetarian diet can be beneficial to human health and be one of the effective preventive strategies for the two most impactful chronic diseases on human health in the 21st century."

Diet and Weight Loss
Diseases and Conditions
Colon Cancer
Endangered Plants
Veterinary Medicine
Colorectal cancer
Ovarian cancer
Polyphenol antioxidant
Stomach cancer
Cervical cancer
HPV vaccine
Breast cancer

Story Source:

Materials provided by PLOS . Note: Content may be edited for style and length.

Journal Reference :

Angelo Capodici, Gabriele Mocciaro, Davide Gori, Matthew J. Landry, Alice Masini, Francesco Sanmarchi, Matteo Fiore, Angela Andrea Coa, Gisele Castagna, Christopher D. Gardner, Federica Guaraldi. Cardiovascular health and cancer risk associated with plant based diets: An umbrella review . PLOS ONE , 2024; 19 (5): e0300711 DOI: 10.1371/journal.pone.0300711

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The 25 Essential Pasta Dishes to Eat in Italy

Two chefs, one cookbook author, a culinary historian and a food writer made a list of the country’s most delicious meals, from carbonara in Rome to ravioli in Campania.

Credit... Enea Arienti

Supported by

By Deborah Dunn , Vicky Bennison , Marianna Cerini , Robyn Eckhardt , Laurel Evans , Kristina Gill , Andrew Sean Greer , Lee Marshall , Elizabeth Minchilli , Marina O’Loughlin , Katie Parla , Rachel Roddy , Eric Sylvers and Laura May Todd

Photographs by Enea Arienti

May 17, 2024

For a food that begins with just flour, water or sometimes eggs, there are infinite variations of pasta. So what happens when you convene a panel of five Italian cuisine experts and ask them to determine the 25 most essential pasta dishes throughout Italy? “I’m sweating,” said Davide Palluda, the chef and owner of All’Enoteca restaurant and osteria in the Piedmont region. “This is too heavy,” he joked during the two-hour video call that I convened to debate his nominations and those of the four other panelists: Stefano Secchi, the chef and a co-owner of New York City’s Rezdôra ; the Tuscany-based cookbook author Emiko Davies ; the Umbria-based culinary historian Karima Moyer-Nocchi ; and the food writer and novelist Roberta Corradin, who lives in Florence, Sicily and Boston. A week before our call, I’d asked each to make their own list of 10 standouts (since he was a panelist, Palluda’s restaurants were automatically excluded); after an energetic debate and several more phone calls, emails and WhatsApp messages, we whittled that list in half. The final picks appear below in unranked alphabetical order, along with the ideal wine to drink with each pasta dish, as recommended by the chosen restaurants and reviewed by Davies’s husband, the sommelier Marco Lami.

This list is the latest in our T 25 series , which highlights significant achievements in the worlds of design, literature , fashion, architecture and food . Previous debates about where to eat right now were confined to major cities like Paris and Mexico City , but this time around, we wanted to see what we might learn if we surveyed the culinary landscape across an entire food-crazed country. We chose pasta because it’s the food most associated with Italy, and because it’s the subject of T’s new Travel issue . It’s also the staple that reveals just how much Italian cooking, even in 2024, remains firmly anchored to a specific place. While most countries have regional fare, Italy is particularly fixated on a recipe’s exact provenance — the town, the valley, the strip of coastline — which is why you’ll often find different pasta shapes or sauces, even over the span of just a few miles.

This culinary diversity informed many of the panelists’ decisions: sometimes, they opted to include a dish because it’s rarely made beyond its birthplace (see Lombardy’s pizzoccheri, No. 12); other times, they chose a favorite sauce (for example, carbonara) or simply a type of pasta like strangozzi (typical of Umbria) since it, like so many local specialties found in the countryside, is paired with different ingredients depending on the time of year.

Only two specific dishes were nominated by more than one panelist: the agnolotti del plin at Madonna della Neve in the Piedmont and the vincisgrassi at Osteria dei Fiori in the Marche region, both centuries-old dishes served at decades-old restaurants. The classics, in general, came up again and again. Even the more idiosyncratic dishes that merited inclusion were riffs on familiar fare: Secchi, for example, made an impassioned plea for the dish called the Crunchy Part of the Lasagna, the chef Massimo Bottura’s technical take on the beloved casserole, offered at his Francescana restaurant at Maria Luigia in Modena, Emilia-Romagna. “If we’re talking about transcendent pasta experiences, that’s it,” Secchi said. (Lasagna, in fact, made a strong showing on this list, which features three varieties.) Secchi suggested one reason the old favorites took primacy: relentless demand.

Northern and central Italy are also overrepresented, perhaps because that’s where most of the participants are based, though Corradin argued that she could easily make an entire list dedicated to any region. And Palluda worried about omitting gnocchi, though there was some disagreement about whether the dumplings usually made with potato and flour are even considered pasta. But Corradin had the final word: “No. Gnocchi is gnocchi. It’s a different chapter. Next time.” — Deborah Dunn

The interview portion has been edited and condensed.

1. The Agnolotti del Plin at Ristorante Madonna Della Neve

Cessole, piedmont.

A dish of stuffed pasta with a sprig of sage.

Overlooking the Bormida valley, Ristorante Madonna della Neve sits opposite the 16th-century chapel for which it’s named. With large windows framing bucolic views, its classic osteria ambience is echoed in its menu of time-honored dishes. While agnolotti is a term used for many kinds of stuffed pasta, especially in Italy’s northwestern Piedmont region, it’s the agnolotti del plin — penny-size filled pasta that’s named for the pinch with which it’s sealed (“pinch” is plin in the Piedmontese dialect) — that are the real star. The manager, Piermassimo Cirio, whose grandparents opened Ristorante Madonna della Neve in 1952 and who sometimes heads up the kitchen, says that meeting the demand for agnolotti del plin requires a full day of filling and folding each week from a crew of staff and family members. And for many guests, the pasta — which is filled with a mixture of ground veal, pork and rabbit, Parmigiano-Reggiano, rosemary and borage — is, in itself, a multicourse meal. Start with the version served al tovagliolo, meaning on a linen napkin without sauce, allowing the gentle sweetness of the filling’s leafy greens to shine. Follow with agnolotti with sage and butter or, more bracingly, sage and lemon juice (Cirio’s invention). Next, try them with a sauce of Bolognese-ish ragù or, as an alternative, the juices and tender scraps of a beef roast (arrosto). For a final course, order a small bowl of agnolotti doused with Barbera wine. Suggested wine pairing: Isolabella della Croce Maria Teresa Barbera d’Asti 2022. — Robyn Eckhardt

2 Reg. Madonna della Neve

Roberta Corradin: I grew up in Piedmont and homemade agnolotti with a roasted meat filling is mandatory.

Karima Moyer-Nocchi: Madonna della Neve is an incredible experience.

Stefano Secchi : I was just there last year and it’s fantastic.

Davide Palluda: I took a picture with the almost 90-year-old [Piera Cirio, Piermassimo’s mother] a few years ago, and I asked her how many agnolotti she’s made in her life. I think a million. She has the forearms! She’s the one that [reminds] all the young chefs in Piedmont why we have to respect [the traditions]. The nicest way to have it is just boiled and naked, without sauce.

Moyer-Nocchi: Oh, yeah, that’s gorgeous. It’s homey and nurturing, and that humble way that it’s served makes it a transformative experience.

2. The Busiate at Duomo

Ragusa ibla, sicily.

The Sicilian chef Ciccio Sultano calls the busiate, an elegant but sturdy corkscrew pasta shape that was historically formed by wrapping the dough around knitting needles (or the stem of a local grass) , “matriarchal.” It’s a specialty of Trapani, on Sicily’s west coast, and usually served with pesto Trapanese: almonds, basil, garlic, tomatoes, pecorino, perhaps a touch of fresh mint. But at Duomo, a gastronomic institution in Ragusa Ibla, on the southern end of the island, Sultano goes much further, imbuing the pasta (always made in-house from heritage grains such as tumminia and perciasacchi) with intense local flavors. The busiate on the current menu features fragrant wild fennel and saffron and a ragù of glittering anchovies and mackerel. And to finish: grated red tuna heart. Another longtime favorite version, which resurfaces from time to time, is the busiate kneaded with rosewater and topped with plump, sweet Mazara prawns (pictured above). Opened nearly 24 years ago, Duomo, as the name suggests, sits in a handsome townhouse down the street from Ragusa Ibla’s dramatic Baroque cathedral, less than an hour from where Sultano took his first job in a kitchen, at a pastry shop, when he was just 13. Eating this dish, he suggests, evokes the island life, culinary influences via Sicily’s many centuries of invaders, from the Greeks and Arabs to the Normans, and the voluptuousness of a cuisine born of the sea. Suggested wine pairing: Pietradolce Archineri Etna Bianco 2018. — Marina O’Loughlin

31 Via Capitano Bocchieri

Corradin: Busiate are Sicily’s version of fusilli. In the western part of Sicily, they make long busiate, which are difficult to eat. If you’re a gentleman, the busiate will slap your tie. That’s the kind that Ciccio Sultano at Duomo makes. The rosewater he puts in the dough gives a hint of the region’s past, when it was under Arab domination. It bounces you back to another time.

3. The Cacio e Pepe at Roscioli Salumeria con Cucina

Made with only pasta, cheese and pepper, cacio e pepe seems downright simple, yet this classic Roman dish is mired with potential pitfalls: cooks know to beware the dreaded clumping. Not only does Roscioli Salumeria con Cucina make a perfect version, they’re unafraid to tweak it when necessary: If the pecorino is fresher, and so less intensely salty, the chefs use only that. If it’s older, they’ll perhaps add some Parmesan to temper the ferocity. Their special blend of ground black peppercorns — including the perfumed, potent Sarawak — makes this simple dish, prepared with tonnarelli (a spaghetti-like egg pasta), memorable. This, at a mere 20 years old, is one of the newer additions to the small Roscioli group of restaurants and bakeries in Rome (a pasticceria also opened 10 years ago). All are popular among tourists, but escaping the chaos of Campo dei Fiori for a seat at the counter here, a glass of red wine in hand, the cacio e pepe in front of you, feels like the real Rome. Suggested wine pairing: Damiano Ciolli Podere Ciriolino Cesanese di Olevano 2022. — M.O.

21 Via dei Giubbonari

Palluda: Cacio e pepe is easy to prepare but it’s not easy to make a good one. Roscioli cooks it the right way, with the right ingredients. If I have the chance I always go when I’m in Rome — if I can get in, it’s a small restaurant — and I always eat the cacio e pepe.

4. The Carbonara at Ristorante l’Arcangelo

Though Rome is the Italian city most often associated with antiquity, carbonara — arguably the most popular of its classic pastas, which also include cacio e pepe, amatriciana and alla gricia — is actually a 20th-century innovation. The dish’s creator and exact place of origin are unknown, but an often-told story involves the arrival of Allied troops in Rome in 1944: The soldiers, or someone cooking for them, allegedly mixed eggs, powdered milk and bacon with pasta. Today, carbonara is usually made with eggs, guanciale (cured pork jowl), pecorino cheese, black pepper and spaghetti. Some chefs use only yolks while others add the whole egg. Some stick to pecorino while others mix in parmigiano. Some pair the sauce with rigatoni instead of spaghetti. Every chef in the city likely believes they make the best version, but the rigatoni alla carbonara at Ristorante l’Arcangelo — a white-tableclothed establishment near Vatican City — has earned its place among the essential dishes of Rome. The silky sauce, salty but not overpowering, evenly coats the rigatoni, pooling just enough in the bottom of the plate so you can dip a piece of bread at the end. The fresh eggs give the dish a vivid yellow hue, and the hefty, crisp pieces of guanciale are doled out with precision; it’s said that the chef personally counts the seven pieces allotted to each plate. Suggested wine pairing: Tenute Filippi Ipazia 2022. — Kristina Gill

59 Via Giuseppe Gioachino Belli

Moyer-Nocchi: I was really torn between including [head chef of Ristorante l’Arcangelo] Arcangelo Dandini’s carbonara or Nabil Hadj Hassen’s. When Nabil was the chef at Salumeria Roscioli, he won a national competition, in 2008, for the best carbonara in Rome. He left Roscioli after 18 years and now he’s at Baccano [also in Rome]. It was a close call between Dandini and Hassen. Post-Covid, when everyone was sitting around thinking about what they were going to do with their lives, Arcangelo made adjustments to the cheeses he uses in the dish. He now uses 80 percent Pecorino Romano sourced locally, from a particular milking. And he’s added 20 percent smoked pecorino di Gavoi from Sardinia, which for him recalls the time when smoking was one of the ways of preserving foods. And he uses these eggs — you’re going to have to trust me — these are just outstanding eggs with the creamiest egg yolks ever. He’s a miraculously inventive chef in the way that he pulls history into his modern iterations of dishes.

Corradin: The carbonara is very good at Arcangelo, and it’s in Prati, a nice bourgeois neighborhood that I believe is also home to several kosher restaurants. It isn’t a place for tourists. Well, in Rome tourists are everywhere, but this is a classic location for real Roman families.

5. The Crunchy Part of the Lasagna at Francescana at Maria Luigia

San damaso, emilia-romagna.

Though it’s served with a fork and spoon, it’s hard to keep your hands off the chef Massimo Bottura’s famous recreation of the coveted corner slice of lasagna. The crispy tower begs to be broken apart with your fingers, the rich ragù and aerated béchamel scooped up, nacho-like, from the plate. To make the dish, Bottura boils spaghetti and then purées it to form a dough, which is divided into three parts, each mixed with a different sauce: basil, Parmigiano-Reggiano or tomato. After being rolled out, the pasta sheets are fried, smoked, and, finally, lightly charred with a torch. The result is somehow both familiar and disorienting: “It’s about feeding people with emotions,” Bottura says. Originally, he served his postmodern take on the homey favorite at his Osteria Francescana , which opened in 1995, but these days it’s available only at Francescana at Maria Luigia , one of the restaurants at Casa Maria Luigia, the guesthouse he opened with his wife, Lara Gilmore, in 2019 in San Damaso, just outside the city of Modena. Here, the sole offering is a nine-course tasting menu comprising Bottura’s well-known dishes, served at communal tables facing an open kitchen. Suggested wine pairing: Comte Lafond Sancerre 2022. — Laurel Evans

56 Stradello Bonaghino

Secchi: I’m biased because I worked at Francescana and I know what it takes [to prepare this lasagna]. It takes three or four days to make. That ragù alone isn’t just made with traditional beef: There’s cheek and side, tongue and a special ingredient I can’t name because Massimo [Bottura] would kill me.

Palluda: Especially in the last 15 years, Massimo Bottura never stops talking about his region, Emilia-Romagna. One of the things he always says is to make good food in Italy, you have to stay with your feet on the land and your brain in the clouds. In his dishes with ragù, you can feel this point of view. Like a lot of guys in Emilia, he probably grew up with the smell of [the sauce] in the house. It’s very important that someone as famous as Bottura still talks about his ingredients and his history — it makes the people and the producers of that region really proud of their home.

6. The Culurgiones at Hotel Ristorante Ispinigoli

Dorgali, sardinia.

From April until October, Hotel Ristorante Ispinigoli serves reimagined Sardinian classics overlooking a patchwork of terraced vineyards, olive groves and fruit orchards that descend toward the Gulf of Orosei on the east coast of Italy’s second-largest island. Among the restaurant’s specialties are culurgiones, fresh pasta parcels filled with a blend of potato, cheese, garlic and mint that are pinched closed, the seams resembling ears of wheat. Native to the Ogliastra subregion of Sardinia that’s about a 90-minute drive south, culurgiones have transcended their hyperlocal origins and are now served across the island, though the filling proportions change from cook to cook. At Hotel Ristorante Ispinigoli, the chef Giovanni Cossu, along with the chef Gian Nicola Mula, leads a multigenerational family-run kitchen that plates them in a novel way: They don’t toss and coat their culurgiones with tomato sauce in the rustic fashion but rather crown each with a spoonful, then top with a dusting of pecorino. Suggested wine pairing: Cantina Tani Taerra Vermentino di Gallura 2022. — Katie Parla

125 Strada Statale

Secchi: This restaurant has been in the family for three generations. It’s about an hour and a half from where my family is from and it has one of the best views in Sardinia. One of the chefs [the nephew of the head chef Cossu] used to work at Osteria Francescana [see No. 5]. He’s cooking traditional pasta, but also doing contemporary things because of his time at high-end restaurants on mainland Italy. I thought he’d go chase the stars, but it’s just the opposite — he wanted to bring everything he learned back home.

7. The Mezzanelli Alla Genovese at Coco Loco

Genoa, the city that lends its name to this meaty pasta sauce, is a good 400 miles from Naples, the place best known for it. Every local seems to have a different origin story for the dish, including the tale that credits Swiss mercenaries for bringing this slow-cooked beef and onion sauce to the southern Italian city sometime around 1495. Though it’s commonly ladled onto short cylindrical pasta shapes such as paccheri or rigatoni, at Coco Loco, which opened in the middle of Naples’s historic center in 1995, the chef and owner, Diego Nuzzo, prefers to use mezzanelli, a longer, skinnier version of ziti. He models his Genovese after the recipe used by monzù, private cooks to the city’s aristocracy in the 18th and 19th centuries who applied French culinary techniques to regional ingredients. Like the monzù, Nuzzo braises the beef shank and lots of red onions in lard rather than olive oil, intensifying the flavor of both ingredients. He then adds white wine, a few cubes of pork and simmers the sauce for up to five hours, adding a little tomato paste toward the end “just to give a touch of color.” But the real secret to the dish, he says, is to choose a dried pasta that doesn’t release too much starch (he prefers the Garofalo brand) to keep the sauce from getting too gluey. Suggested wine pairing: Quintodecimo Terra d’Eclano Irpinia Aglianico 2015. — Lee Marshall

4 Vicoletto Cappella Vecchia

Palluda: It’s difficult to explain to people that this is a [Neapolitan] dish and the name Genovese only refers to the people who moved from Genoa to Napoli. In Genoa, you usually get a pesto condimento [sauce]. Here, it’s a lot of meat and the protagonist of this recipe is the onions. You just color the onion with tomatoes.

Corradin: It’s one of the many geographically confusing dishes in Italian cuisine — like zuppa inglese; inglese means “English” and it’s not English at all. And it’s not a soup at all, it’s dessert. [We call them] false friends.

Moyer-Nocchi: It’s a fabulous dish. That five-hour braise renders something that tastes like a sweet, beef-flavored onion butter that loses whatever negative connotations onions have and becomes a larger-than-the-sum-of-its-parts dish. Diego Nuzzo is the most renowned for [pasta alla Genovese] and [he serves it] in a really elegant setting.

Corradin: And unlike most pastas, in Napoli, pasta alla Genovese is served as a main course.

8. The Minestra di Pasta Mista With Shellfish and Rockfish at La Torre del Saracino

Vico equense, campania.

A meal at La Torre del Saracino, in the seaside town of Vico Equense, is something of a ceremony. It begins in a Medieval watchtower overlooking the Bay of Naples where you’re welcomed with an aperitif (a sparkling Franciacorta, for example) and small bites (perhaps a free range-chicken cacciatora panino) while listening to music chosen by guests from the chef Gennaro Esposito’s vinyl collection, with plenty of 20th-century Neapolitan pop and jazz. Then you’re led down a winding stone staircase to a 20-seat main dining room with high arched windows overlooking the sea. The minestra di pasta mista con crostacei e pesci di scoglio, one of Esposito’s signature dishes, is a nod to the fish soup that the 54-year-old chef, a native of Vico Equense, grew up eating. In those days, it was made mostly with the catch that couldn’t be sold at the markets and typically took hours to prepare. Now, at La Torre del Saracino, it’s a symbol of gleeful abundance: Esposito uses more than a pound and a half of Mediterranean rockfish, shrimps, squid and prawns to make one portion. Still one of the more time-consuming dishes in his repertoire, it involves slow-cooking the rockfish in a light fish stock, then squeezing them in a French duck press to retain the juices. Once all the seafood and San Marzano tomatoes are left to simmer on the stove top, for several hours, he adds a mix of as many as 15 different pasta shapes, both tubes and spirals (families traditionally made minestre like this to use up those annoying bottom-of-the-package leftovers). The pasta is left to cook in the soup so that, in Esposito’s words, “it absorbs all its goodness.” Suggested wine pairing: Mastroberardino Stilema Fiano di Avellino 2015. — L.M.

9 Via Torretta

Palluda: Gennaro Esposito is one of the new generation of chefs from Campania, from Napoli. Twenty-five years ago, it wasn’t so easy to introduce new ideas in Campania — it seemed like you were fighting with tradition, but that’s not why he did it. He learned a lot of new techniques in France [and elsewhere] and then used products that were close to him. He made new recipes without losing the identity of the original one. A lot of young chefs followed him. His minestra pasta is a very interesting dish. You mix in a lot of types of pasta. Every spoonful is different. Like chocolate, you never know what you’re going to get. It’s a very rustic dish, but very technical.

9. The Orecchiette With Broccoli at Ricci Osteria

If you find yourself wandering the whitewashed back streets of a Pugliese town, you’ll likely encounter women gathered near the stoops of their houses, forming semolina flour dough into quarter-size orecchiette, which they leave to dry on netted boxes balanced atop wooden stands. Shaped vaguely like an earlobe (the name translates to little ear) orecchiette is often served with ragù or turnip greens, but among the most beloved variations is one made with broccoli. In Milan, some 550 miles to the north of Italy’s heel, the chefs Antonella Ricci and Vinod Sookar have created their own version of the recipe at the Pugliese-inflected mainstay Ricci Osteria, which opened in 2022. Usually, the dish is made by sautéing parboiled broccoli with garlic, anchovies and mildly spicy pepperoncini in extra virgin olive oil; theirs also includes sweet, soft confit tomatoes. The finishing flourish is a generous sprinkling of crunchy toasted bread crumbs, which serve as the ideal foil to the orecchiette’s chewy texture. Suggested wine pairing: a 2020 negroamaro from Agricola Felline. — Laura May Todd

27 Via Pasquale Sottocorno

Moyer-Nocchi.: Antonella Ricci is from Puglia and her husband and partner in the restaurant [Vinod Sookar] is from Mauritius. And together they really represent Milan. [The city] is a micro-melting pot in Italy that since the end of World War II has pulled in a great exodus from the rural south, because that’s where the jobs were, and then later, a great influx of people of Sri Lankan and Indian origin. It’s good to see a person of color in the position of chef as well, because Italy’s restaurants would not go on without this population.

Palluda : It’s a dish made with briciole [breadcrumbs], which is something you usually throw away. They call it the poor man’s Parmesan. And with these scraps, they’ve built this amazing dish.

10. The Paccheri Alla Vittorio at Da Vittorio

Brusaporto, lombardy.

What happens when a restaurant with such fine-dining pedigree takes on pasta with tomato sauce, one of the simplest of all the primi? You get a creamy, almost velvety rendition that’s become the calling card for Da Vittorio, a luxurious fixture of the northern city of Bergamo since 1966. In the early 2000s, Vittorio Cerea and his family, including his son, the current head chef, Enrico “Chicco” Cerea, moved the restaurant from the historic core of the city to a villa surrounded by parkland, less than five miles outside of town. From there, Enrico expanded the menu, offering innovative dishes like scampi with fermented miso and tempura sardines with a lemon sauce. But diners who come from Milan — about 30 miles to the southwest — and much farther (there’s a heliport and a hotel on the property) often have just one item on their mind: the paccheri alla Vittorio. A cork-size tubular pasta, paccheri are served here slightly al dente and swimming in a sauce made with three types of tomatoes, basil, olive oil and sautéed garlic, thickened at the end with butter and Parmesan. The dish, offered as part of an eight-course tasting menu, also comes with a bib — you’re invited to mop up the sauce with freshly baked farro bread. Suggested wine pairing: Vie di Romans Chardonnay 2020. — Eric Sylvers

17 Via Cantalupa

Palluda: It’s cooked like risotto, meaning that you cook it for just 80 percent of the time in the water, and then you finish the dish directly in the [sauce], and they do that at the table in front of the people.

Secchi: [They serve] it convivio, family-style, which is a beautiful way to do it.

Moyer-Nocchi: What makes the dish so worthy of this list is the sauce. My advice: Opt for the bib.

11. The Pasta con le Sarde at Trattoria Ferro di Cavallo

Palermo, sicily.

When your massive portion of pasta con le sarde at Trattoria Ferro di Cavallo in Palermo is set in front of you, your first thought is likely, “What is this mess of gloopy spaghetti covered with greenish-brown sauce?” But it’s precisely the dish’s aggressively ugly appearance that makes the first bite — and smell — so surprising. The rustic recipe is full of all the contradictions and complexities inherent to Sicilian cooking: High-end ingredients like plump sweet raisins and resinous pine nuts mix with sardines, the poorest of fish, barely boned, to form more of a stew than a pasta sauce; it’s also redolent of wild fennel. The warm, chaotic Trattoria Ferro di Cavallo, which opened in 1944 and is in the heart of the old city, doesn’t take reservations, but with the two big rooms inside, and the large covered terrace outside, you’ll rarely have to wait long. Suggested wine pairing: Tasca d’Almerita Regaleali Bianco 2022. — Elizabeth Minchilli

20 Via Venezia

Moyer-Nocchi: Pasta con le sarde doesn’t get as much attention as it should. Ferro di Cavallo puts a lot of care into it. They have an investment in the tradition of this dish. It’s a very colorful, classic trattoria.

12. The Pizzoccheri at Ristorante Quattro Stagioni

Mantello, lombardy.

Some pasta dishes demand you put aside restraint. Pizzoccheri certainly qualify — the fettuccine-like buckwheat pasta is typically tossed together with copious amounts of Valtellina Casera cheese and butter, potatoes and a vegetable (usually cabbage). Said to be born at least 200 years ago at the foot of the Alps in Valtellina — a valley that runs east from the northern shores of Lake Como — the hearty dish is still the perfect thing to eat at Quattro Stagioni, with its exposed beams, simple wooden chairs and stone fountain in the middle of the main dining room. The restaurant is part of the La Fiorida agriturismo, a working farm that doubles as a country inn, with 29 guest rooms, some 500 animals (mainly cows, goats and sheep), a cheese-making facility and 150 acres of cultivated fields. While the buckwheat is sourced from a nearby farm, nearly everything else used in the pizzoccheri comes from on site. This means that, depending on the time of year, you might find spinach or Swiss chard in your pizzoccheri. “There is no exact recipe because it’s always changing,” says the head chef, Gianni Tarabini. Suggested wine pairing: Nino Negri Inferno Valtellina Superiore 2019. — E.S.

12 Via Lungo Adda

Moyer-Nocchi: Very few pasta dishes use non-wheat flours but the pizzoccheri of Valtellina, made with mostly buckwheat, has been awarded European Union P.G.I. [Protected Geographical Indication] certification, bringing it into the panoply of Italy’s most highly valued traditional dishes. It’s a deeply comforting pasta.

Davies: I love pizzoccheri.

Palluda: I just don’t know if American people know about pizzoccheri.

Davies: Maybe that’s why it should be on the list.

Moyer-Nocchi: La Fiorida makes an excellent pizzoccheri, and it’s a beautiful agriturismo. Very small, local everything.

13. The Rasnal Soup at Maggese

San miniato, tuscany.

The faded grocery store sign still hangs above the door of Maggese in the ancient Tuscan hill town of San Miniato. Step into the small retro-modern interior, glance to the right and there, behind a two-seater counter, you’ll usually find Fabrizio Marino, fielding orders and greeting clients. Opening a vegetarian restaurant in meat-oriented Tuscany back in 2019 was a risk, Marino admits. But he needn’t have worried: Maggese books out days in advance. Rasnal — which he says means “of the Etruscans” — is a soup that’s been a fixture on the Maggese menu from the beginning. It pairs slow-braised seasonal vegetables — some foraged, some cultivated — like wild asparagus and artichoke with a sauce of local red heirloom beans. The dish’s pasta component consists of just four simple, bite-size eggless-pasta parcels made from heirloom flour. Their fillings can change with the seasons — they might be celeriac or chickpeas, pumpkin or carrot — but they always deliver a sweet note to balance the broth’s bitterness. Suggested wine pairing: Il Borghetto Montigiano Sangiovese 2019. — L.M.

29 Via IV Novembre

Davies : I love everything that they do at this restaurant. It’s in my town, San Miniato. We’re in the middle of a place that is very, very well known for red meat. They used to have seven butcher shops in this small town.

Palluda: They eat the vegans there.

Davies: When Maggese opened, it was like this breath of fresh air because everything they do is vegetarian. The owner and head chef [Marino] is from a nearby town and there are a few Japanese chefs [in his kitchen], and they often use ingredients like miso within their dishes. Not in a really obvious way; you just get this little kick of umami. This minestra [reminds me] of pasta e fagioli. When it arrives at the table, the pasta and the soup are separate so you can tip the pasta into the soup or you can eat them separately. It’s a joy.

14. The Ravioli With Ricotta, Walnuts and Burnt Garlic at Oasis Sapori Antichi

Vallesaccarda, campania.

Since the day it opened in 1988, Oasis Sapori Antichi, in the rural town of Vallesaccarda, a two-hour drive east of the Amalfi Coast, has had ravioli with ricotta, walnuts and burnt garlic on the menu. It’s a dish of happenstance: Founder Giuseppina Fischetti neglected a pan on the stovetop and a sauce was born. This could so easily be another accidental origin story, charming but entirely forgettable; but, more than three decades later, it’s become the cornerstone of an exceptional kitchen. Now in the hands of Giuseppina’s five children and grandchildren (both in the kitchen and front of house), Oasis Sapori Antichi focuses primarily on the ingredients grown just outside town, in the territory of Irpinia with its great natural resources. The garlic used in their sauce — toasted, rather than burnt, until it has a savory toffee-like flavor — is blended with the area’s malizia walnuts and olive oil produced by the Fischetti family less than a mile from the front door. The ravioli is also made daily and filled with local cow’s milk ricotta and flecks of minced parsley. The restaurant itself looks like a slightly theatrical living room, with its scattering of Persian rugs and tall candlesticks. But while the service is formal and elegant, the family’s natural ease warms the room. Suggested wine pairing: Boccella Rosa Taurasi Aglianico 2015. — Rachel Roddy

8/10 Via Provinciale

Corradin: The garlic tastes more smoky than burnt. I first had it 14 years ago, and I spent part of my life thinking about when I could go back. I’ve been back several times since.

Palluda: No one has said that to me in my life.

Corradin: The dream of each and every chef.

15. The Spaghetti all’Assassina at Al Sorso Preferito

Bari, puglia.

A few years ago, if you had asked anyone outside of Bari about spaghetti all’Assassina they’d have given you a blank stare. The dish was so specific to the capital of Puglia that only one or two restaurants served it. The method, which was handed down to Pierino Lonigro, the owner of the town’s Al Sorso Preferito, by the supposed inventor of this dish, in the 1960s, involves cooking the spaghetti into a tomato sauce filled with pepperoncini until the mixture forms a crust that’s spicy and slightly crispy. It’s a difficult technique to get right, but Lonigro credits his well-seasoned cast-iron pan that he’s been using for decades. He bought the restaurant in 1974; that same year, he moved it to its current location in the elegant Murat neighborhood. Most locals start with the mixed antipasto, an array of raw and cooked seafood, before having the Assassina. Legend has it that the name of this dish came from the fact that the spiciness of the sauce almost killed customers, though Lonigro’s version, a nice balance of sweetness and mild heat, presents very little danger. Suggested wine pairing: Paololeo Alture Susumaniello 2020. — E.M.

40 Via Vito Nicola De Nicolò

Moyer-Nocchi: While the concept is easy enough, it takes an experienced hand to produce the desired effect: crispy, fiery spaghetti. Al Sorso Preferito may be an unassuming, few-frills restaurant, but it’s the mecca for this dish.

16. The Spaghettone all’Amatriciana at Santo Palato

When you order spaghettone all’amatriciana at Santo Palato near the Basilica di San Giovanni in Rome, the servers tell you that it will take at least 15 minutes. This is both a courtesy and reassurance that the thick spaghetti will be boiled to order, not always the case in a city where, more often than you might imagine, the reliance on precooked pasta keeps service swift, but means the dishes can often lack texture. Santo Palato is a small trattoria, simply furnished and decorated with Futurist-style posters, the daily specials chalked-up on a blackboard. The chef and owner, Sarah Cicolini, sources the spaghettone from a Roman pasta maker called Pastificio Lagano, and the jarred cherry tomatoes from Agricola Paglione, a farm in Puglia. The pigs’ cheek guanciale and the sheep’s milk Pecorino Romano cheese she chooses are also from small producers. One of the four canonical Roman pasta dishes, amatriciana is the sum of these four parts, which Cicolini — often visible through an opening into the kitchen — brings together expertly. Suggested wine pairing: Cantina Ribelà Saittole 2020. — R.R.

4 A/B Piazza Tarquinia

Secchi: When I first went there, about seven years ago, Sarah was one of the very few women in this new avant-garde of Roman chefs, and she was cooking offal, which had always been butch men territory.

Moyer-Nocchi: Santo Palato is a seamless combination of an old trattoria and modern design and it reflects Sarah’s approach to the way she reconceptualizes traditional Roman food.

Secchi: She cooks all the four classic Roman pastas and she does it damn well.

17. The Squash Tortelli at Dal Pescatore Santini

Runate, lombardy.

Tortelli di zucca, a winter squash stuffed pasta, is made a little differently throughout Lombardy but perfected at Dal Pescatore, outside of Mantova (the dish’s supposed birthplace), in the village of Runate. Much can go wrong with this seasonal pasta (at its best in autumn), from the inclusion of amaretti cookies at some places to the addition of strange, mustardy candied fruits at others; it can be too sweet, too spicy, too sour or otherwise unbalanced. Perhaps worst of all, the dish can be oversauced, with a creamy topping drowning out the flavor and texture of the pasta. But at Dal Pescatore, the chefs Nadia and Giovanni Santini have made tortelli the centerpiece: from the slight bite of the outer rim to the tender interior that encloses the filling. The five pieces they provide — which aren’t so much coated with as touched by butter and Parmigiano-Reggiano — are just enough. Suggested wine pairing: Ca’ del Bosco Annamaria Clementi Franciacorta 2015. — Andrew Sean Greer

15 Riserva del Parco Oglio Sud

Secchi: It’s in the middle of nowhere, but they have a helicopter pad there, so people from Milano fly in and have dinner. That place is an institution.

Corradin: The first time I went to Dal Pescatore, Nadia realized I was sick and she cooked me tortellini en brodo [tortellini in broth]; after that, I could’ve eaten a 25-course meal. But I agree with Stefano that the iconic dish there is tortelli di zucca.

18. The Strangozzi at Enoteca L’Alchimista

Montefalco, umbria.

At first glance, strangozzi looks like spaghetti. But unlike that more ubiquitous pasta, which tends to originate in factories, the slightly chubbier strangozzi are hand-rolled, hand-pulled and mostly found in central Italy. At L’Alchimista, established in 2001 in the medieval Umbrian hill town of Montefalco, the chef and co-owner Patrizia Moretti makes it the old-fashioned way: with just water and extra-fine “00” wheat flour, which makes them pleasantly chewy. Go in the warm weather and you’ll likely be seated at an outdoor table in what might be one of Italy’s prettiest piazzas. This, too, is the time of year Moretti serves the pasta with tender greens foraged from nearby fields or with a pesto, made from two of the greens and wild garlic. If you come in summer, you might find your plate of strangozzi tossed with zucchini and in fall, topped with black truffles. Suggested wine pairing: a young trebbiano Spoletino from Tenuta Bellafonte. — E.M.

14 Piazza del Comune

Davies: When I was last there, there was a strangozzi with wild herbs — [ones] no one will have ever heard of that you collect in the Umbrian countryside. It’s just a very simple dish but it’s special . One is called strigoli and another is vitalba, whose English names are not very appetizing (bladder campion and old man’s beard). They’re herbs that need to be picked young and have been foraged for centuries — it’s a really ancient sort of dish.

19. The Tagliolino Cacio e Burro at Cibrèo Caffè

Cibrèo Caffè, the more informal outpost of a small, influential group of restaurants near Mercato Sant’Ambrogio (the locals’ preferred traditional food market), opened in 1983, and it’s still one of Florence’s most inviting places to stop in for a negroni and a snack (say, a pizzetta). But those in the know head straight for the cacio e burro. Here, the ultimate comfort food — pasta doused in melted butter and cheese — is approached with the same earnestness you might expect of fussier fare: Butter, Parmigiano-Reggiano and hot milk are blended together with enough force that it forms a paste, which melts into a cream on contact with the hot pasta — at Cibrèo, it’s tagliolini, the narrower, more delicate sibling of tagliatelle. Its yolk-yellow color, and faint sweetness, comes from the unlikely addition of boiled carrots into the purée. Suggested wine pairing: Podere Erica l’Erica Rosé Sangiovese 2022‌. — M.O.

5r Via Andrea del Verrocchio

Corradin: If we mention Cibrèo, we have to mention the tagliolino cacio e burro.

Secchi: Oh, I agree.

Emiko Davies: Cibrèo is my go-to restaurant in Florence. My husband worked there, as the head sommelier, but he doesn’t anymore. The cacio e burro is still one of my favorite dishes there. Fabio Picchi [the founder of Cibrèo who died in 2022] cheekily called it “rubato,” stolen, because it’s a revisitation of another iconic Florentine dish, the taglierini gratinati from Harry’s Bar, a favorite since the 1950s.

20. The Tagliolini With Lobster at Ristorante Cecio

Corniglia, liguria.

Set atop a steep hill on a particularly dramatic stretch of Italian coastline, Corniglia is considered the quietest of the touristy Cinque Terre villages. When you finally reach town, after climbing a 382-step brick stairway up a rocky cliff from the train station (or taking the shuttle bus), you’ll be ready for a large plate of pasta. Ristorante Cecio in Corniglia — which has been family owned and operated since 1976 — is the place to find it. The menu revolves around local seafood that’s sourced daily and pasta dishes by the head chef, Gabriele Pittavini, who’s honed his craft over the 20 years he spent operating a fresh pasta shop. One favorite is the tagliolini all’astice, a thin, homemade egg pasta with lobster, available for a minimum of two people. At first glance, it’s a flamboyant dish: a cherry-red claw reaches straight up from the ribbons of pasta, adorned with fat morsels of pink meat and a sprinkling of parsley. Half a lobster fills one side of the plate. Upon tasting it, however, you’ll find it showcases the fresh ingredients without overembellishing them. Be sure to reserve a table outside: The view from the veranda alone justifies a visit. Suggested wine pairing: Cinque Terre DOC 2023. — L.E.

58 Via Serra

Davies: I’ve been going here with my family for well over a decade — we love the Cinque Terre but it’s changed a lot and this trattoria has always stayed the same. The seafood is incredibly fresh. There’s nothing like a summertime dinner there.

21. The Tajarin al Ragù at Osteria da Gemma

Roddino, piedmont.

Gemma Boeri has been hand-rolling and cutting tajarin pasta for the locals in Roddino, a small town in southern Piedmont, for almost four decades. “Why would I stop? This is what I know how to do,” she says. The large glass window connecting the dining area of her hilltop trattoria with the prep room affords a view of Boeri and her helpers preparing the long, skinny strands of egg pasta (similar to spaghetti but with a golden hue), while the outside-facing windows overlook the Langhe hills known for producing quality food and wine, including Barolo. Boeri serves the tajarin (the Piedmontese word for tagliolini, a thinner version of tagliatelle) with a thick beef ragù sauce, which she says has won over diners because it reminds them of the comfort food they enjoyed when they were kids. “There’s no secret, I just prepare the food like nonna used to,” she says. It can take several months to get a reservation. Yet da Gemma has nonetheless remained relaxed and unpretentious: its walls lined with photos dating back to when Boeri first started serving customers in 1986. She serves only a single fixed menu that, in addition to the tajarin, includes Piedmontese classics, such as beef tartare and agnolotti del plin, the area’s signature stuffed pasta (see No. 1). Suggested wine pairing: Agricola Gianpiero Marrone La Pantalera Barbera d’Alba Superiore 2020. — E.S.

6 Via Guglielmo Marconi

Palluda: Every month I go see Gemma just to kiss her hand. It’s true, I’m not joking. She’s our pope.

Secchi: Her place is in the mountains. It’s very hard to get to, and it’s very blue-collar. When you sit down to eat, everything is served family-style, and the amount of food that comes to your table is … I mean, completely unnecessary. Gemma is like the original nonna. A few times a week, all the nonnas in the village come to roll pasta with her, and then they all sit down together for lunch. How does that tradition carry on when her time passes? There’s got to be a way.

22. The Tortelloni With Ricotta, Parmesan and Butter at Hosteria Giusti

Modena, emilia-romagna.

Salumeria Giusti , in operation since at least 1605, is reported to be the world’s oldest delicatessen, but that’s not its only claim to fame. Beyond the antique wood and marble counter a hallway leads to a tiny dining room with only four tables. Reservations here are among Modena’s most coveted, especially after the restaurant, a favorite of locals for decades, was featured on the Netflix series “Master of None” in 2017. Daniele Morandi, whose grandparents opened Hosteria in 1989, is in charge of the pasta making. He rolls out each sheet of dough by hand with a long wooden pin and shapes every raviolo and tortellino with skill and speed he learned from his grandmother. Among his most popular offerings are tortelloni — pillowy larger versions of typical Modenese tortellini — filled with a mix of local ricotta, aged Parmigiano-Reggiano, spinach and freshly grated nutmeg. Bathed in an emulsion of pasta water and unpasteurized French butter, the dish is a study in simplicity. (Lunch only, though dinner can be prearranged for groups of 12 or more.) Suggested wine pairing: Corte d’Aibo Spungola Sauvignon Blanc 2022. — L.E.

75 Via Luigi Carlo Farini

Secchi: I worked there when I first moved to Modena, but only after I went to 30 different places to taste fresh pasta. In terms of technique and ambience, Giusti blew my mind. And that tortelloni? I think the ricotta is still warm when it’s delivered to the kitchen. It just disintegrates in your mouth.

23. The Traditional Lasagna at Al Cambio

Bologna, emilia-romagna.

In a bland, busy neighborhood not far from Bologna’s exhibition center, Al Cambio has been drawing a business crowd during weekday lunches and couples and families for dinner and on weekends for the past three decades. After booking weeks in advance, they file into the spare, white and beige dining room, debate the offerings on the extensive wine list (dominated by varieties from the Emilia-Romagna region) and settle in for a long lunch or dinner of local specialties, from breaded veal cutlets and mortadella to sformatino (a type of potato soufflé). But the most ordered — and scrutinized — dish is the one that bears the city’s name: lasagna alla Bolognese. Like most places in town, Al Cambio offers a seven-layer lasagna made with jade-green spinach noodles sandwiched between coats of béchamel and ragù. But Al Cambio’s ragù is meatier than most, made with beef minced together with prosciutto and pork sausage, and then topped with a thick layer of the ragù, the “final flourish,” as the manager Piero Pompili says: “It’s our way of symbolizing Bologna’s food heritage.” Suggested wine pairing: San Patrignano Avi Sangiovese di Romagna Superiore Riserva 2019. — Vicky Bennison

150 Via Stalingrado

Stefano Secchi: People are going to have a lot of opinions about where to find the best [lasagna alla Bolognese in Bologna], but for me, this is it. It has the perfect amount of crispness and gooeyness.

24. The Trofie With Pesto at Antica Osteria di Vico Palla

Pesto alla Genovese — the pungent bright green sauce made from basil, extra-virgin olive oil, Parmigiano-Reggiano, pecorino, pine nuts, garlic and salt — can be tossed with almost any shape of pasta, from spaghetti to fusilli. Its most authentic pairing, however, is trofie, a short, hand-twisted noodle typical of Recco , just down the coast from Genoa. It’s here that the most commonly known pesto originated (what’s thought to be the earliest printed recipe appeared in the 1863 book “La Cuciniera Genovese”), and at Antica Osteria di Vico Palla the dish is served at its most elemental. The rustic restaurant — where patrons sit at simple wooden tables laid with brown paper place mats under vaulted brick ceilings that date back to the 1500s — serves its trofie pesto mixed with boiled potatoes and green beans, as local families have for generations. The menu changes daily; ask for this dish if you don’t see it. Suggested wine pairing: a young vermentino di Albenga from the Ligurian coast. — Marianna Cerini

15/r Vico Palla

Palluda: You can’t have a list of Italian dishes without pesto. It’s the most popular condimento in the world. It’s very light, it’s modern, and it’s easy to make. If you want to blend it, instead of making it with a mortar, and you want to make a good, lively pesto, you really should have cold ingredients.

Corradin : In Genoa, poor people added potatoes and green beans to their pasta with pesto to make it a piatto unico, richer in nutrients but still affordable. [It’s common] to eat it scarpetta, the Italian ritual of scraping up the remaining sauce with bread. But here you use potatoes instead of bread. The beauty of this kind of dish and this kind of trattoria is that they’re both reminders that, in Italy, you don’t have to be rich to enjoy a good meal.

25. The Vincisgrassi at Osteria Dei Fiori

Macerata, marche.

Tourists tend to flock to Macerata, a small hilltop city in the eastern part of the Marche region, for two reasons: The summer opera festival and the decidedly unsummery seven-layer baked pasta dish known as vincisgrassi. Letizia Carducci, one of the three siblings who have been running the 30-seat Osteria Dei Fiori, which opened in 1980 on a cobblestone street close to the main square, says the dish evolved from princisgras, a pasta casserole made with black truffles and prosciutto that was served to the local nobility in the 18th century. In the Marcerate province, resourceful housewives made a ragù using meat from various farmyard animals, including bones and offal; that’s the recipe that Iginia and her brother, Paolo (they cook; their sister Letizia is the maitre’d), have built on to make their vincisgrassi, which consists of duck, chicken, rabbit and a little pork. Dessert wine, vino cotto, also plays a key role: It’s added to the dough that the Carduccis knead into silk-thin pasta sheets, then used to saute the chicken and duck livers, which are stirred into the sauce at the very end. The meaty ragù covers the four bottom layers, while the top one is reserved for the nutmeg-inflected béchamel sauce. Baked in an oven, the whole thing is both earthy and luxurious, with subtle hints of smoke. Suggested wine pairing: Gàjole Verdicchio di Matelica 2021. — V.B.

61 Via Lauro Rossi

Secchi: What is vincisgrassi? I’ve never had it.

Corradin: It’s Macerata’s ancestral lasagna. One story says that it’s named for an Austrian officer named Windisch-Graetz who was stationed in Macerata province around the early 1800s.

Moyer-Nocchi: Lasagna has become a specific dish, associated with a specific place. The Maceratese prefer not to call their dish a lasagna, even though it, too, is a rich, layered pasta dish.

Palluda: When these dishes were born, there were no computers [people didn’t sit all day] and no radiators. They stayed warm with a fire, but with the food also. They expended calories to stay warm. People ate just one meal every day.

Moyer-Nocchi: Historically, you’d only eat these things once or twice a year. It’s not like you’d be picking these dishes off a menu every day. In the meantime, you’d be eating much more frugally: cabbage, beans, leafy greens.

Palluda: Somebody said to me, “Why don’t you make some of these traditional pastas lighter?” But that’s not the right way to respect the dishes. We can make the portions smaller, but you need to keep the flavor.

Photo editor: Lauren Poggi

Research editor: Alexis Sottile

Copy editor: Magnus Schaefer

An earlier version of this article misidentified the restaurant where Nabil Hadj Hassen was the chef in 2008; it was Salumeria Roscioli, not Antico Forno Roscioli.

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

Cover of The Health Consequences of Involuntary Exposure to Tobacco Smoke

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

1 introduction, summary, and conclusions.

Introduction

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

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

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

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

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

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

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

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

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

Table 1.3. Selected major reports, other than those of the U.

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

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

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

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

Organization of the Report

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

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

Preparation of the Report

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

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

Definitions and Terminology

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

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

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

Evidence Evaluation

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

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

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

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

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

Major Conclusions

This report returns to involuntary smoking, the topic of the 1986 Surgeon General’s report. Since then, there have been many advances in the research on secondhand smoke, and substantial evidence has been reported over the ensuing 20 years. This report uses the revised language for causal conclusions that was implemented in the 2004 Surgeon General’s report ( USDHHS 2004 ). Each chapter provides a comprehensive review of the evidence, a quantitative synthesis of the evidence if appropriate, and a rigorous assessment of sources of bias that may affect interpretations of the findings. The reviews in this report reaffirm and strengthen the findings of the 1986 report. With regard to the involuntary exposure of nonsmokers to tobacco smoke, the scientific evidence now supports the following major conclusions:

Secondhand smoke causes premature death and disease in children and in adults who do not smoke.
Children exposed to secondhand smoke are at an increased risk for sudden infant death syndrome ( SIDS ), acute respiratory infections, ear problems, and more severe asthma. Smoking by parents causes respiratory symptoms and slows lung growth in their children.
Exposure of adults to secondhand smoke has immediate adverse effects on the cardiovascular system and causes coronary heart disease and lung cancer.
The scientific evidence indicates that there is no risk-free level of exposure to secondhand smoke.
Many millions of Americans, both children and adults, are still exposed to secondhand smoke in their homes and workplaces despite substantial progress in tobacco control.
Eliminating smoking in indoor spaces fully protects nonsmokers from exposure to secondhand smoke. Separating smokers from nonsmokers, cleaning the air, and ventilating buildings cannot eliminate exposures of nonsmokers to secondhand smoke.
Chapter Conclusions

Chapter 2 Toxicology of Secondhand Smoke

Evidence of carcinogenic effects from secondhand smoke exposure.

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

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

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

Mechanisms of Secondhand Smoke Exposure and Heart Disease

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

Chapter 3. Assessment of Exposure to Secondhand Smoke

Building designs and operations.

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

Exposure Models

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

Biomarkers of Exposure to Secondhand Smoke

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

Chapter 4. Prevalence of Exposure to Secondhand Smoke

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

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

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

Pregnancy (Spontaneous Abortion and Perinatal Death)

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

Infant Deaths

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

Sudden Infant Death Syndrome

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

Preterm Delivery

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

Low Birth Weight

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

Congenital Malformations

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

Cognitive Development

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

Behavioral Development

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

Height/Growth

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

Childhood Cancer

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

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

Lower respiratory illnesses in infancy and early childhood.

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

Middle Ear Disease and Adenotonsillectomy

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

Respiratory Symptoms and Prevalent Asthma in School-Age Children

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

Childhood Asthma Onset

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

Lung Growth and Pulmonary Function

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

Chapter 7. Cancer Among Adults from Exposure to Secondhand Smoke

Lung cancer.

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

Breast Cancer

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

Nasal Sinus Cavity and Nasopharyngeal Carcinoma

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

Cervical Cancer

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

Chapter 8. Cardiovascular Diseases from Exposure to Secondhand Smoke

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

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

Odor and irritation.

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

Respiratory Symptoms

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

Lung Function

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

Chronic Obstructive Pulmonary Disease

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

Chapter 10. Control of Secondhand Smoke Exposure

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

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

Classification of Secondhand Smoke Exposure

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

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

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

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

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

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

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

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

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

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

Misclassification of Secondhand Smoke Exposure

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

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

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

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

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

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

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

Use of Meta-Analysis

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

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

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

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

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

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

Confounding

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

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

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

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

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

Tobacco Industry Activities

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

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

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Cite this Page Office on Smoking and Health (US). The Health Consequences of Involuntary Exposure to Tobacco Smoke: A Report of the Surgeon General. Atlanta (GA): Centers for Disease Control and Prevention (US); 2006. 1, Introduction, Summary, and Conclusions.
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Introduction. Tobacco use is well established as a major cause of death worldwide, accounting for about five to six million deaths per year worldwide (Jha and Peto, 2014).On current smoking patterns, about one billion deaths may occur from smoking during the 21 st century, in contrast to 'only' 100 million deaths in the 20 th century (Peto et al., 1994).
The 25 Essential Pasta Dishes to Eat in Italy
Two chefs, one cookbook author, a culinary historian and a food writer made a list of the country's most delicious meals, from carbonara in Rome to ravioli in Campania.
1 Introduction, Summary, and Conclusions
The topic of passive or involuntary smoking was first addressed in the 1972 U.S. Surgeon General's report (The Health Consequences of Smoking, U.S. Department of Health, Education, and Welfare [USDHEW] 1972), only eight years after the first Surgeon General's report on the health consequences of active smoking (USDHEW 1964). Surgeon General Dr. Jesse Steinfeld had raised concerns about ...
Federal Register, Volume 89 Issue 98 (Monday, May 20, 2024)
[Federal Register Volume 89, Number 98 (Monday, May 20, 2024)] [Rules and Regulations] [Pages 44144-44461] From the Federal Register Online via the Government Publishing Office [www.gpo.gov] [FR Doc No: 2024-08568] [[Page 44143]] Vol. 89 Monday, No. 98 May 20, 2024 Part IV Department of Labor ----- Occupational Safety and Health Administration ----- 29 CFR Part 1910 Hazard Communication ...