Using the Past to Understand the Future of U.S. and Global Smoking Disparities: A Birth Cohort Perspective

Tam, Jamie; Levy, David T.; Feuer, Eric J.; Jeon, Jihyoun; Holford, Theodore R.; Meza, Rafael

doi:10.1016/j.amepre.2022.12.003

Cited by 6 publications

(2 citation statements)

References 76 publications

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“…Chronic stress, targeted industry marketing, peer influences, and frequent exclusion from prevention messages all likely contribute to increased tobacco use susceptibility. Incarcerated populations similarly have skyrocketing smoking rates (up to 80-90% in some facilities) attributable to stress, secondhand smoke exposure, and unrestricted access to tobacco products in many correctional settings (Tam et al 2023).…”

Section: Disparities In Smokingmentioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

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Background Tobacco smoking remains a major preventable cause of disease and death worldwide. Combustible cigarettes release thousands of chemicals that can initiate inflammatory pathways leading to smoking-related illness. This review aims to synthesize current scientific knowledge on mechanisms of smoking-induced disease, epidemiological trends, and clinical strategies from recent literature. Main body of the abstract At the cellular level, cigarette smoke triggers oxidative stress through reactive oxygen species (ROS), causing DNA damage. This provokes inflammatory signaling cascades mediated by damage-associated molecular patterns (DAMPs), receptors like RAGE and TLRs, and downstream cytokines. Smoking also disrupts apoptosis and autophagy. In the lungs, oxidative stress and inflammation from smoking play central roles in COPD pathogenesis. Smoking-induced oxidative DNA damage, chronic inflammation, and impaired immunity combine to promote lung carcinogenesis. For cardiovascular disease, smoking triggers endothelial dysfunction, platelet activation, and atherogenesis through oxidized LDL and effects on nitric oxide and adhesion molecules. Short conclusion Given the unequivocal evidence of health risks, smoking cessation is critical to reducing preventable death and disability. Both counseling and pharmacotherapy have proven efficacy for quitting, but efficacy remains limited long-term. Emerging nicotine products like e-cigarettes have unknown impacts on cessation and population health. Comprehensive efforts encompassing prevention, screening, treatment innovation, harm reduction, and policy reform focused on curbing smoking-attributable morbidity and mortality are warranted.

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Section: Disparities In Smokingmentioning

confidence: 99%

Oxidative stress and inflammation: elucidating mechanisms of smoking-attributable pathology for therapeutic targeting

Addissouky,

El Sayed,

Ali

et al. 2024

Bull Natl Res Cent

View full text Add to dashboard Cite

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“…Although Brazil has a nationwide surveillance system tracking tobacco use—which many LMICs lack—when data are not collected annually or with set frequencies, the absence of information presents challenges for time-series analyses and forecasting. The validated APC methodology pioneered by CISNET, already extended to numerous U.S. populations, 24 , 25 , 28 , 34 , 46 – 50 has been adapted for Brazil, allowing a thorough investigation of trends in smoking because they have varied across cohorts and time.…”

Section: Discussionmentioning

confidence: 99%