Estimating the Health Impacts of Tobacco Harm Reduction Policies: A Simulation Modeling Approach

With adult smoking prevalence rates declining too slowly to reach national objectives, opinion leaders are considering policies to improve tobacco-related outcomes by regulating the composition of cigarettes to be (1) less harmful and/or (2) less addictive. Because harm reduction efforts may actually encourage higher cigarette consumption by promoting a safer image, and addictiveness reduction may increase the harmfulness of cigarettes by encouraging compensatory smoking behaviors, policymakers must consider the tradeoffs between these two approaches when proposing legislation to control cigarette content. To estimate health impacts, we developed a dynamic computer model simulating changes in the age- and gender-specific smoking behaviors of the U.S. population over time. Secondary data for model parameters were obtained from publicly available sources. Population health impacts were measured as change in smoking prevalence and the change in cumulative quality-adjusted life-years (QALYs) in the U.S. population over 75 years. According to the risk-use threshold matrix generated by the simulation, modifying cigarettes to reduce their harmfulness and/or addictiveness could result in important gains to the nation's health. Addictiveness reduction efforts producing a 60% improvement in smoking behavior change probabilities would produce a net gain in population health at every plausible level of increase of smoking-related harm that was modeled. A 40% reduction in smoking-related harm would produce a net QALY gain at every level of behavior change considered. This research should prove useful to policymakers as they contemplate giving the FDA the authority to regulate the composition of cigarettes.     

Influence of Risk Perception on Attitudes and Norms Regarding Electronic Cigarettes

The use of electronic cigarettes has grown substantially over the last few years. Currently, about 4% of adults use electronic cigarettes, about 16% of high school students report use in the past 30 days, as do approximately 11–25% of college students. A hallmark of the reduction in tobacco use has been the shift in social norms concerning smoking in public. Such norms may also drive views on acceptability of public electronic cigarette use. While normative factors have been given attention, little substantive application of the literature on risk perception has been brought to bear. The overall aim of this study was to place a cognitive–affective measure of risk perception within a model that also includes social cues for e‐cigarettes, addictiveness beliefs, and tobacco use to predict perceived social acceptability for public use of e‐cigarettes. To do so, a cross‐sectional study using an online survey was conducted among a sample of undergraduate students at a Western university (n = 395). A structural equation model showed that the acceptability of public e‐cigarette use was influenced by social cues, beliefs about addiction, and cognitive risk perception, even after controlling for nicotine use. What is revealed is that cognitive assessment of e‐cigarette risk and perception of addictiveness had a suppressing effect on perceived acceptability of public vaping, while greater exposure to social cues exerted a countervailing effect. This is evidence of the role that risk perception and social norms may play in the increases in electronic cigarette use that have been observed.     

Exposure to Environmental Tobacco Smoke in the Workplace and the Impact of Away-From-Work Exposure

Concentrating on exposure in workplaces where smoking occurs, we examined environmental tobacco smoke (ETS)-related concentration data from the 16-City Study.^(1,2) This study involved a large population of nonsmokers, used personal monitors, and encompassed a wide selection of ETS-related constituents. This first article in a series of three describes the 16-City Study, considers the impact of demographic variables, and concludes that these variables did not explain differences in exposure to ETS. We compared 16-City Study concentrations obtained in the workplace to previously reported workplace concentrations and determined that data from this study were representative of current ETS exposure in nonmanufacturing workplaces where smoking occurs. Considering factors other than demographic factors, we found that, not surprisingly, the number of cigarettes observed in the workplace had an impact on exposure concentrations. Finally, we compared people from homes where smoking occurs with people from nonsmoking homes and found that people from smoking homes observed more smoking in the workplace and experienced higher concentrations of ETS-related compounds in the workplace, even when they observed the same number of cigarettes being smoked in the workplace. In two subsequent articles in this series, we discuss relationships between various ETS markers and provide estimates of distributions of doses to nonsmoking workers employed in workplaces where smoking occurs.     

Estimation of the Leukemia Risk in Human Populations Exposed to Benzene from Tobacco Smoke Using Epidemiological Data

Several epidemiological studies have demonstrated an association between occupational benzene exposure and increased leukemia risk, in particular acute myeloid leukemia (AML). However, there is still uncertainty as to the risk to the general population from exposure to lower environmental levels of benzene. To estimate the excess risk of leukemia from low‐dose benzene exposure, various methods for incorporating epidemiological data in quantitative risk assessment were utilized. Tobacco smoke was identified as one of the main potential sources of benzene exposure and was the focus of this exposure assessment, allowing further investigation of the role of benzene in smoking‐induced leukemia. Potency estimates for benzene were generated from individual occupational studies and meta‐analysis data, and an exposure assessment for two smoking subgroups (light and heavy smokers) carried out. Subsequently, various techniques, including life‐table analysis, were then used to evaluate both the excess lifetime risk and the contribution of benzene to smoking‐induced leukemia and AML. The excess lifetime risk for smokers was estimated at between two and six additional leukemia deaths in 10,000 and one to three additional AML deaths in 10,000. The contribution of benzene to smoking‐induced leukemia was estimated at between 9% and 24% (U_pperCL 14–31%). For AML this contribution was estimated as 11–30% (U_pperCL 22–60%). From the assessments carried out here, it appears there is an increased risk of leukemia from low‐level exposure to benzene and that benzene may contribute up to a third of smoking‐induced leukemia. Comparable results from using methods with varying degrees of complexity were generated.     

CSP Deposition to the Alveolar Region of the Lung: Implications of Cigarette Design

Ventilated cigarettes were designed to reduce the levels of smoke under machine testing conditions; however, smokers alter their smoking pattern to compensate for the reduction in yields. A relative shift in incidence of lung cancer from the more central lung airways to the alveolar region has also been associated with ventilated cigarette use. Validated mathematical models indicate that particle deposition patterns in the lung depend on particle size and inhalation behavior, including inhalation volume, flow rate, and breath-hold time. This article finds that most mathematical models underpredict total cigarette smoke particulate (CSP) deposition in the lung, likely because they do not account for coagulation, hygroscopicity, and cloud dynamics, which may increase the effective particle diameter of CSP reaching the lung tissue. The models that include these processes indicate that puff volume would be unlikely to affect particle deposition in the lung, but puff time, inhalation depth, breath-hold time, and exhalation time may affect total deposition. Most compensation appears to occur through a combination of increased puff volume and puff flow, with possible increases in inhalation depth and breath-hold time. The complex interaction between the extent of cigarette ventilation, which can affect puffing/inhalation behavior, CSP concentration, and CSP size with CSP dose to the alveolar versus more central lung airways is described. Deposition efficiency in the alveoli could plausibly be increased through compensation, but it is still unclear whether compensation could sufficiently alter patterns of CSP deposition in the lung to elicit a shift in lung cancer sites.     

Cigarette Smoking and Multiple Health Risk Behaviors: A Latent Class Regression Model to Identify a Profile of Young Adolescents

Cigarette smoking is often established during adolescence when other health‐related risk behaviors tend to occur. The aim of the study was to further investigate the hypothesis that risky health behaviors tend to cluster together and to identify distinctive profiles of young adolescents based on their smoking habits. To explore the idea that smoking behavior can predict membership in a specific risk profile of adolescents, with heavy smokers being more likely to exhibit other risk behaviors, we reanalyzed the data from the 2014 Health Behaviour in School‐Aged Children Italian survey of about 60,000 first‐ and third‐grade junior high school (JHS) and second‐grade high school (HS) students. A Bayesian approach was adopted for selecting the manifest variables associated with smoking; a latent class regression model was employed to identify smoking behaviors among adolescents. Finally, a health‐related risk pattern associated with different types of smoking behaviors was found. Heavy smokers engaged in higher alcohol use and abuse and experienced school failure more often than their peers. Frequent smokers reported below‐average academic achievement and self‐rated their health as fair/poor more frequently than nonsmokers. Lifetime cannabis use and early sexual intercourse were more frequent among heavy smokers. Our findings provide elements for constructing a profile of frequent adolescent smokers and for identifying behavioral risk patterns during the transition from JHS to HS. This may provide an additional opportunity to devise interventions that could be more effective to improve smoking cessation among occasional smokers and to adequately address other risk behaviors among frequent smokers.     

Assessment of Interindividual and Geographic Variability in Human Exposure to Fine Particulate Matter in Environmental Tobacco Smoke

Environmental tobacco smoke (ETS) is a major contributor to indoor human exposures to fine particulate matter of 2.5 μm or smaller (PM_2.5). The Stochastic Human Exposure and Dose Simulation for Particulate Matter (SHEDS‐PM) Model developed by the U.S. Environmental Protection Agency estimates distributions of outdoor and indoor PM_2.5 exposure for a specified population based on ambient concentrations and indoor emissions sources. A critical assessment was conducted of the methodology and data used in SHEDS‐PM for estimation of indoor exposure to ETS. For the residential microenvironment, SHEDS uses a mass‐balance approach, which is comparable to best practices. The default inputs in SHEDS‐PM were reviewed and more recent and extensive data sources were identified. Sensitivity analysis was used to determine which inputs should be prioritized for updating. Data regarding the proportion of smokers and “other smokers” and cigarette emission rate were found to be important. SHEDS‐PM does not currently account for in‐vehicle ETS exposure; however, in‐vehicle ETS‐related PM_2.5 levels can exceed those in residential microenvironments by a factor of 10 or more. Therefore, a mass‐balance‐based methodology for estimating in‐vehicle ETS PM_2.5 concentration is evaluated. Recommendations are made regarding updating of input data and algorithms related to ETS exposure in the SHEDS‐PM model. Interindividual variability for ETS exposure was quantified. Geographic variability in ETS exposure was quantified based on the varying prevalence of smokers in five selected locations in the United States.     

Approximations for Estimating Change in Life Expectancy Attributable to Air Pollution in Relation to Multiple Causes of Death Using a Cause Modified Life Table

There is considerable debate as to the most appropriate metric for characterizing the mortality impacts of air pollution. Life expectancy has been advocated as an informative measure. Although the life‐table calculus is relatively straightforward, it becomes increasingly cumbersome when repeated over large numbers of geographic areas and for multiple causes of death. Two simplifying assumptions were evaluated: linearity of the relation between excess rate ratio and change in life expectancy, and additivity of cause‐specific life‐table calculations. We employed excess rate ratios linking PM_2.5 and mortality from cerebrovascular disease, chronic obstructive pulmonary disease, ischemic heart disease, and lung cancer derived from a meta‐analysis of worldwide cohort studies. As a sensitivity analysis, we employed an integrated exposure response function based on the observed risk of PM_2.5 over a wide range of concentrations from ambient exposure, indoor exposure, second‐hand smoke, and personal smoking. Impacts were estimated in relation to a change in PM_2.5 from 19.5 μg/m³ estimated for Toronto to an estimated natural background concentration of 1.8 μg/m³. Estimated changes in life expectancy varied linearly with excess rate ratios, but at higher values the relationship was more accurately represented as a nonlinear function. Changes in life expectancy attributed to specific causes of death were additive with maximum error of 10%. Results were sensitive to assumptions about the air pollution concentration below which effects on mortality were not quantified. We have demonstrated valid approximations comprising expression of change in life expectancy as a function of excess mortality and summation across multiple causes of death.     

Car Occupant Life Expectancy: Car Mass and Seat Belt Effects

Average human life expectancies for the U.S. resident population are calculated using tabulated population and survival rate data. These life expectancies are recalculated assuming elimination of various types of motor vehicle fatalities using Fatal Accident Reporting System (FARS) data. The differences between the original and recalculated values provide estimates of life expectancy reductions due to the motor vehicle fatalities. These estimates are combined with prior work relating the likelihood of an occupant fatality to car mass, so that reductions in life expectancy are determined as a function of car mass. The estimates of life expectancy reductions are also used to determine the effect of seat belt use on life expectancy. The estimates, which are based on data for 1978, assume that survival rates remain unchanged. Estimates of the changes in life expectancy associated with switching from a large (1800 kg) car to a small (900 kg) car, and switching from not using to using a seat belt are presented as functions of the age at which an individual makes the switch.     

Health-Based Population Forecasting: Effects of Smoking on Mortality and Fertility

A microsimulation model, allowing one to forecast short- and long-term population changes conditional on the prevalence of a risk factor in a population, is presented. In this model, population changes result from the aggregation of changes in individual event histories, which, in turn, result from mortality and infertility rates recalculated in accordance with their known relative risks in population groups exposed to a risk factor. Smoking, being the most widespread and influential preventable public health risk factor, is chosen to demonstrate the abilities of the model to forecast the population effects of different hypothetical smoking prevalences. The demographic and population health effects on 20-, 50-, and 100-year projections with the current, hypothetically doubled, and hypothetically halved the current smoking prevalence are analyzed in detail. The model predicts an increase in life expectancy (0.99 year for males and 0.64 years for females), and an increase in population size (2.2-7.5% dependent on the age group) if smoking prevalence is reduced by half. Sensitivity analyses of all findings are performed. The generalization of the model to account for multiple risk factors (e.g., the simultaneous effects of alcohol consumption, obesity, and smoking) and effects on medical expenditures are discussed.     

Environmental Tobacco Smoke Revisited: The Reliability of the Data Used for Risk Assessment

Several epidemiological studies have found a weak, but consistent association between lung cancer in nonsmokers and exposure to environmental tobacco smoke (ETS). In addition, a purported link between such exposure and coronary heart disease (CHD) has been of major concern. Although it is biologically plausible that ETS has a contributory role in the induction of lung cancer in nonsmoking individuals, dose-response extrapolation-supported by the more solid database for active smokers-gives an additional risk for lung cancer risk that is more than one order of magnitude lower than that indicated by major positive epidemiological studies. The discrepancy between available epidemiological data and dosimetric estimates seems, to a major part, to reflect certain systematic biases in the former that are difficult to control by statistical analysis when dealing with risks of such low magnitudes. These include, most importantly, misclassification of smoking status, followed by inappropriate selection of controls, as well as certain confounding factors mainly related to lifestyle, and possibly also hereditary disposition. A significant part of an association between lung cancer and exposure to ETS would disappear, if, on the average, 1 patient out of 20 nonsmoking cases had failed to tell the interviewer that he had, in fact, recently stopped smoking. In the large International Agency for Research on Cancer (IARC) multicenter study even lower misclassification rates would abolish the weak, statistically nonsignificant associations that were found. In the former study an apparent significant protective effect from exposure to ETS in childhood with respect to lung cancer later in life was reported, a most surprising finding. The fact that the mutation spectrum of the p53 tumor suppressor gene in lung tumors of ETS-exposed nonsmokers generally differs from that found in tumors of active smokers lends additional support to the notion that the majority of tumors found in ETS-exposed nonsmokers have nothing to do with tobacco smoke. The one-sided preoccupation with ETS as a causative factor of lung cancer in nonsmokers may seriously hinder the elucidation of the multifactorial etiology of these tumors. Due to the high prevalence of cardiovascular disease in the population, even a modest causal association with ETS would, if valid, constitute a serious public health problem. By pooling data from 20 published studies on ETS and heart disease, some of which reported higher risks than is known to be caused by active smoking, a statistically significant association with spousal smoking is obtained. However, in most of these studies, many of the most common confounding risk factors were ignored and there appears to be insufficient evidence to support an association between exposure to ETS and CHD. Further, it seems highly improbable that exposure to a concentration of tobacco smoke at a level that is generally much less than 1% of that inhaled by a smoker could result in an excess risk for CHD that-as has been claimed-is some 30% to 50% of that found in active smokers. There are certainly valid reasons to limit exposure to ETS as well as to other air pollutants in places such as offices and homes in order to improve indoor air quality. This goal can be achieved, however, without the introduction of an extremist legislation based on a negligible risk of lung cancer as well as an unsupported and highly hypothetical risk for CHD.     

Longevity and Lifetime Labor Supply: Evidence and Implications

Conventional wisdom suggests that increased life expectancy had a key role in causing a rise in investment in human capital. I incorporate the retirement decision into a version of Ben‐Porath's (1967) model and find that a necessary condition for this causal relationship to hold is that increased life expectancy will also increase lifetime labor supply. I then show that this condition does not hold for American men born between 1840 and 1970 and for the American population born between 1890 and 1970. The data suggest similar patterns in Western Europe. I end by discussing the implications of my findings for the debate on the fundamental causes of long‐run growth.     

A Method for Comparing the Impact on Carcinogenicity of Tobacco Products: A Case Study on Heated Tobacco Versus Cigarettes

Comparing the harmful health effects related to two different tobacco products by applying common risk assessment methods to each individual compound is problematic. We developed a method that circumvents some of these problems by focusing on the change in cumulative exposure (CCE) of the compounds emitted by the two products considered. The method consists of six steps. The first three steps encompass dose-response analysis of cancer data, resulting in relative potency factors with confidence intervals. The fourth step evaluates emission data, resulting in confidence intervals for the expected emission of each compound. The fifth step calculates the change in CCE, probabilistically, resulting in an uncertainty range for the CCE. The sixth step estimates the associated health impact by combining the CCE with relevant dose-response information. As an illustrative case study, we applied the method to eight carcinogens occurring both in the emissions of heated tobacco products (HTPs), a novel class of tobacco products, and tobacco smoke. The CCE was estimated to be 10- to 25-fold lower when using HTPs instead of cigarettes. Such a change indicates a substantially smaller reduction in expected life span, based on available dose-response information in smokers. However, this is a preliminary conclusion, as only eight carcinogens were considered so far. Furthermore, an unfavorable health impact related to HTPs remains as compared to complete abstinence. Our method results in useful information that may help policy makers in better understanding the potential health impact of new tobacco and related products. A similar approach can be used to compare the carcinogenicity of other mixtures.     

Radon as a Tracer of Lung Changes Induced by Smoking

After smoking, exposure to radon and its progeny is the second leading cause of lung cancer. The probability of inducing lung carcinomas by inhaled radon progeny depends on the deposited radiation dose, and is significantly affected by physiological and morphometric changes induced by smoking. Due to irritation of the airways, the inhalation of cigarette smoke leads to the hyperproduction of mucus. Two concurrent processes occur: on one hand, increased production of mucus protects the target cells against radiation damage; on the other hand, in the case of long-term smokers, a chronic lung obstruction develops, causing an increase in the radiation dose to the lungs. Depending on the duration and intensity of smoking, these processes contribute to the final radiation dose with different weights. The primary objective of this study was to investigate to what extent these smoke-induced changes can modify the resulting absorbed dose of inhaled radon progeny relative to healthy nonsmokers. Since the bronchial dose depends on the degree of lung tissue damage, we have used this dose as a tool for detecting the effects of smoking on the lung epithelium. In other words, the biological effect of radon served as a tracer of changes induced by smoking.     

Risk Assessment and Alternatives Assessment: Comparing Two Methodologies

The selection and use of chemicals and materials with less hazardous profiles reflects a paradigm shift from reliance on risk minimization through exposure controls to hazard avoidance. This article introduces risk assessment and alternatives assessment frameworks in order to clarify a misconception that alternatives assessment is a less effective tool to guide decision making, discusses factors promoting the use of each framework, and also identifies how and when application of each framework is most effective. As part of an assessor's decision process to select one framework over the other, it is critical to recognize that each framework is intended to perform different functions. Although the two frameworks share a number of similarities (such as identifying hazards and assessing exposure), an alternatives assessment provides a more realistic framework with which to select environmentally preferable chemicals because of its primary reliance on assessing hazards and secondary reliance on exposure assessment. Relevant to other life cycle impacts, the hazard of a chemical is inherent, and although it may be possible to minimize exposure (and subsequently reduce risk), it is challenging to assess such exposures through a chemical's life cycle. Through increased use of alternatives assessments at the initial stage of material or product design, there will be less reliance on post facto risk‐based assessment techniques because the potential for harm is significantly reduced, if not avoided, negating the need for assessing risk in the first place.     

Estimating the Risks of Smoking, Air Pollution, and Passive Smoke on Acute Respiratory Conditions

Five years of the annual Health Interview Survey, conducted by the National Center for Health Statistics, are used to estimate the effects of air pollution, smoking, and environmental tobacco smoke on respiratory restrictions in activity for adults, and bed disability for children. After adjusting for several socioeconomic factors, the multiple regression estimates indicate that an independent and statistically significant association exists between these three forms of air pollution and respiratory morbidity. The comparative risks of these exposures are computed and the plausibility of the relative risks is examined by comparing the equivalent doses with actual measurements of exposure taken in the homes of smokers. The results indicate that: (1) smokers will have a 55-75% excess in days with respiratory conditions severe enough to cause reductions in normal activity; (2) a 1 microgram increase in fine particulate matter air pollution is associated with a 3% excess in acute respiratory disease; and (3) a pack-a-day smoker will increase respiratory restricted days for a nonsmoking spouse by 20% and increase the number of bed disability days for young children living in the household by 20%. The results also indicate that the estimates of the effects of secondhand smoking on children are improved when the mother's work status is known and incorporated into the exposure estimate.     

Risk Perception Among Smokers: A Qualitative Study

The aim of this qualitative study is to identify the dimensions people used to assess the risk of smoking and then compare them with those used by health professionals in primary healthcare. Five discussion groups were conducted. The field work was carried out in Barcelona (Spain), from February 2005 to January 2006. Data were analyzed following a semantic‐thematic categorical content analysis (ACC‐ts). Results showed that people tend to employ stereotypical discourses when evaluating the risk of smoking. Similarly, they reassess the risk in the context of their life experience and incorporate new nuances to the arguments sustaining their behavior. Once this reassessment takes place, the decision to continue smoking emerges, and smokers come up with additional arguments justifying their habit (i.e., age, benefits related to costs). Professionals are aware of this process and its multidimensional nature. Nevertheless, their discourse loses this multidimensional feature when discussing the strategies they use at smoking cessation interventions. This qualitative study increases the understanding of various meanings that people attribute to their life experience. These assumptions may be useful for developing health practices that are closer to people. As a practical utility of these results, it would be interesting to apply a preliminary assessment of the different meanings that people attribute to smoking from their life context in risk communication.     

Managing Risk as a Duality of Harm and Benefit: A Study of Organizational Risk Objects in the Global Insurance Industry

This study examines how organizations construct and manage risk objects as a duality of harm–benefit within their normal operations. It moves beyond the existing focus on accidents, disasters and crisis. We study the risk‐transfer processes of 35 insurers where they navigate the tension of retaining risk in their insurance portfolio to increase the benefit of making profit and transferring risk to reinsurance to reduce the harm of paying claims. We show that organizations’ constructions of risk are underpinned by everyday risk management practices of centralizing, calculating and diversifying. Through variation in these practices, not all organizations seek balance and we in turn uncover the sensemaking processes of abstracting and localizing that enable organizations to prioritize harm or benefit. This contributes to the risk literature by illuminating the co‐constitutive relationship between risk sensemaking processes and everyday risk management practices. Following the complex linkages involved in the construction of risk objects as sources of harm–benefit, our analysis also contributes to the literature on dualities. It shows that while immediate trade‐offs between harm–benefit occur, prioritizing one element of the duality is ultimately a means for attaining the other. Thus, while initial imbalance is evident, prioritization can be an enabling approach to navigating duality.     

Assessment of the Effectiveness of Radon Screening Programs in Reducing Lung Cancer Mortality

The present study was aimed at assessing the health consequences of the presence of radon in Quebec homes and the possible impact of various screening programs on lung cancer mortality. Lung cancer risk due to this radioactive gas was estimated according to the cancer risk model developed by the Sixth Committee on Biological Effects of Ionizing Radiations. Objective data on residential radon exposure, population mobility, and tobacco use in the study population were integrated into a Monte‐Carlo‐type model. Participation rates to radon screening programs were estimated from published data. According to the model used, approximately 10% of deaths due to lung cancer are attributable to residential radon exposure on a yearly basis in Quebec. In the long term, the promotion of a universal screening program would prevent less than one death/year on a province‐wide scale (0.8 case; IC 99%: –3.6 to 5.2 cases/year), for an overall reduction of 0.19% in radon‐related mortality. Reductions in mortality due to radon by (1) the implementation of a targeted screening program in the region with the highest concentrations, (2) the promotion of screening on a local basis with financial support, or (3) the realization of systematic investigations in primary and secondary schools would increase to 1%, 14%, and 16.4%, respectively, in the each of the populations targeted by these scenarios. Other than the battle against tobacco use, radon screening in public buildings thus currently appears as the most promising screening policy for reducing radon‐related lung cancer.     

Political Corporate Social Responsibility: Reviewing Theories and Setting New Agendas

There has been rising interest in political corporate social responsibility (political CSR), defined as activities where CSR has an intended or unintended political impact, or where intended or unintended political impacts on CSR exist. Based on a survey and content analysis of 146 peer‐reviewed academic articles from 18 journals over the 14‐year period 2000–2013, this paper systematically reviews the existing applications of general theories (such as legitimacy theory, the resource‐based view and Habermasian political theory) within the political CSR literature. The survey indicates that the political CSR field is dominated by institutional theory and stakeholder theory, but future theory development needs to go beyond these theories in order to address a number of critical gaps. This review specifically points to several avenues for future political CSR research with regard to the individual level of analysis, domain integration and political CSR in multinational enterprises. The paper ends with a call for a new theory‐informed and pluralist research agenda on political CSR to integrate different perspectives and re‐examine the role of the state.