抽烟 · 烟在身体里做了什么

参考文献 · 21

1. Valavanidis, A., Vlachogianni, T., & Fiotakis, K. (2009). Tobacco smoke: involvement of reactive oxygen species and stable free radicals in mechanisms of oxidative damage, carcinogenesis and synergistic effects with other respirable particles. International Journal of Environmental Research and Public Health, 6(2), 445-462. Review plus the authors' EPR and spin-trapping lab work. The particulate phase contains at least 3,500 compounds, many toxic, carcinogenic or mutagenic; the gas phase holds an estimated ~10^15 free radicals per puff (after Pryor), formed and destroyed in a steady state and rising as smoke ages; tar holds ~10^17 stable radicals per gram. The tar semiquinone system can redox-cycle; aqueous tar extracts formed the DNA lesion 8-OHdG; hydroxyl-radical generation was synergistic with asbestos, PM2.5 and diesel particles; conventional and haemoglobin 'bio-filters' did not substantially alter the radical content of smoke. Chemistry and cell findings, not measured harm in people (abstract and full text, PMID 19440393). 10.3390/ijerph6020445
2. Pryor, W. A. (1997). Cigarette smoke radicals and the role of free radicals in chemical carcinogenicity. Environmental Health Perspectives, 105(Suppl 4), 875-882. Review. Radicals are probably involved in a substantial number, though probably not a majority, of cancer initiation reactions; promotion always involves radicals to some extent. Aqueous cigarette tar extracts contain a quinone-hydroquinone-semiquinone system that reduces oxygen to superoxide and hence hydrogen peroxide and the hydroxyl radical; the tar radical can penetrate viable cells, bind to DNA and cause nicks. Laboratory chemistry and cell work (abstract, PMID 9255574). 10.1289/ehp.97105s4875
3. Rose, J. J., Wang, L., Xu, Q., McTiernan, C. F., Shiva, S., Tejero, J., & Gladwin, M. T. (2017). Carbon monoxide poisoning: pathogenesis, management, and future directions of therapy. American Journal of Respiratory and Critical Care Medicine, 195(5), 596-606. Review of CO poisoning. Hemoglobin has a 250-fold greater affinity for CO than for oxygen; CO binding stabilizes the high-affinity R-state, so the remaining sites hold oxygen tighter and release less to tissues; CO also binds myoglobin (60-fold greater affinity than oxygen) and cytochrome c oxidase. COHb of 2% or more in nonsmokers and 10% or more in smokers is considered abnormal. Normobaric oxygen cuts the CO elimination half-life from 320 minutes on room air to 74 minutes; hyperbaric oxygen to about 20 minutes. It is about poisoning, not about smoking-level exposure (full text, PMID 27753502; erratum 2017). 10.1164/rccm.201606-1275CI
4. Kallner, A. B., Hartmann, D., & Hornig, D. H. (1981). On the requirements of ascorbic acid in man: steady-state turnover and body pool in smokers. American Journal of Clinical Nutrition, 34(7), 1347-1355. Healthy male volunteers smoking more than 20 cigarettes a day, given a single oral dose of 14C-labelled ascorbic acid at steady-state intakes of about 30-180 mg/day. Smokers had a higher metabolic turnover than nonsmokers; the authors concluded smokers need at least 140 mg/day to reach steady-state concentrations and body pools comparable to nonsmokers, for whom about 100 mg/day had been reported appropriate. Small isotope-tracer study; the later IOM increment for smokers (+35 mg/day) rests on it (abstract, PMID 7258125). 10.1093/ajcn/34.7.1347
5. Institute of Medicine. (2000). Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids. National Academies Press. www.ncbi.nlm.nih.gov/books/NBK225483
6. Tribble, D. L., Giuliano, L. J., & Fortmann, S. P. (1993). Reduced plasma ascorbic acid concentrations in nonsmokers regularly exposed to environmental tobacco smoke. American Journal of Clinical Nutrition, 58(6), 886-890. Cross-sectional: 44 passive smokers, 47 active smokers, 50 unexposed nonsmokers. Plasma ascorbic acid in passive smokers was intermediate between active smokers and unexposed nonsmokers despite similar dietary vitamin C intakes; hypovitaminosis C (< 23 umol/L) in 24% of active and 12% of passive smokers, none of the unexposed. Low plasma levels were associated with low intake only in the smoke-exposed groups. Conclusion: chronic smoke exposure, particularly with low vitamin C intake, may reduce ascorbate pools in both active and passive smokers (abstract, PMID 8249873). 10.1093/ajcn/58.6.886
7. The ATBC Cancer Prevention Study Group. (1994). The effect of vitamin E and beta carotene on the incidence of lung cancer and other cancers in male smokers. NEJM, 330(15), 1029–1035. 29,133 male smokers aged 50-69 in south-western Finland; alpha-tocopherol 50 mg/day, beta-carotene 20 mg/day, both, or placebo; follow-up 5-8 years. Lung cancer: alpha-tocopherol -2% (-14 to 12%), beta-carotene +18% (3 to 36%). Fewer prostate cancers with alpha-tocopherol, more deaths from haemorrhagic stroke; total mortality 8% higher with beta-carotene (abstract, PMID 8127329). 10.1056/NEJM199404143301501
8. Omenn, G. S., et al. (1996). Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease (CARET). NEJM, 334(18), 1150–1155. 10.1056/NEJM199605023341802
9. US Preventive Services Task Force. (2022). Vitamin, mineral, and multivitamin supplementation to prevent cardiovascular disease and cancer: recommendation statement. JAMA, 327(23), 2326–2333. 10.1001/jama.2022.8970
10. Wang, X.-D., Liu, C., Bronson, R. T., Smith, D. E., Krinsky, N. I., & Russell, M. (1999). Retinoid signaling and activator protein-1 expression in ferrets given beta-carotene supplements and exposed to tobacco smoke. Journal of the National Cancer Institute, 91(1), 60-66. Ferrets given a high-dose beta-carotene supplement, cigarette smoke, or both for 6 months. All supplemented animals showed a strong proliferative response and squamous metaplasia in the lung, enhanced by smoke; all three treatment groups had lower lung retinoic acid and 18%-73% lower RAR-beta expression; the combined group had threefold to fourfold higher c-Jun and c-Fos expression. Authors propose diminished retinoid signaling as a mechanism that could enhance lung tumorigenesis after high-dose beta-carotene plus smoke. The other half: their background notes people who eat more fruit and vegetables or have high serum beta-carotene have lower lung cancer risk. Animal study (abstract, PMID 9890171). 10.1093/jnci/91.1.60
11. Audrain-McGovern, J., & Benowitz, N. L. (2011). Cigarette smoking, nicotine, and body weight. Clinical Pharmacology & Therapeutics, 90(1), 164-168. Narrative review. Adult smokers weigh on average 4-5 kg less than nonsmokers; smoking increases 24-h energy expenditure by about 10% (about 200 kcal/day); nicotine acts through central neurotransmitters on appetite-suppressing and metabolism-raising pathways (pro-opiomelanocortin, CART). Post-cessation weight gain comes from a fall in metabolic rate and a rise in intake: in one study quitters ate on average 227 kcal/day more, explaining 69% of the weight gained at 3 months. The other half: the heaviest smokers weigh more than lighter smokers in some studies, and cessation drugs delay rather than prevent the weight gain (full text, PMID 21633341). 10.1038/clpt.2011.105
12. Aubin, H.-J., Farley, A., Lycett, D., Lahmek, P., & Aveyard, P. (2012). Weight gain in smokers after quitting cigarettes: meta-analysis. BMJ, 345, e4439. Meta-analysis of 62 studies (cessation trial arms). In untreated quitters mean weight gain was 1.12 kg at 1 month, 2.26 kg at 2, 2.85 kg at 3, 4.23 kg at 6 and 4.67 kg (95% CI 3.96 to 5.38) at 12 months; most gain occurs within 3 months. Variation is large: at 12 months about 16% lost weight, 37% gained under 5 kg, 34% gained 5-10 kg and 13% gained more than 10 kg. Estimates were similar with different pharmacotherapies and between people concerned and not concerned about weight (abstract, PMID 22782848). 10.1136/bmj.e4439
13. Clair, C., Rigotti, N. A., Porneala, B., Fox, C. S., D'Agostino, R. B., Pencina, M. J., & Meigs, J. B. (2013). Association of smoking cessation and weight change with cardiovascular disease among adults with and without diabetes. JAMA, 309(10), 1014-1021. Framingham Offspring cohort, 3,251 participants, 631 CVD events. Median 4-year weight gain in recent quitters without diabetes was 2.7 kg. Versus smokers, recent quitters had HR 0.47 (0.23-0.94) and long-term quitters 0.46 (0.34-0.63) for CVD, barely changed by adjusting for weight change: a net cardiovascular benefit despite weight gain. The other half: among people with diabetes the point estimates were similar but not statistically significant; observational (abstract, PMID 23483176). 10.1001/jama.2013.1644
14. Sørensen, L. T. (2012). Wound healing and infection in surgery: the pathophysiological impact of smoking, smoking cessation, and nicotine replacement therapy: a systematic review. Annals of Surgery, 255(6), 1069-1079. 177 pathophysiological studies. Smoking temporarily lowers tissue oxygenation and aerobic metabolism; it blunts inflammatory-cell chemotaxis, migration and oxidative bacterial killing, unbalances proteolytic enzymes, and slows fibroblast migration and proliferation and collagen synthesis. Cessation restores tissue oxygenation and metabolism rapidly and inflammatory-cell function in part within 4 weeks, but the proliferative response remains impaired. Nicotine does not affect the tissue microenvironment; nicotine replacement effects appear marginal (abstract, PMID 22566015). 10.1097/SLA.0b013e31824f632d
15. Scanlon, P. D., Connett, J. E., Waller, L. A., Altose, M. D., Bailey, W. C., Buist, A. S., & Tashkin, D. P. (2000). Smoking cessation and lung function in mild-to-moderate chronic obstructive pulmonary disease: the Lung Health Study. American Journal of Respiratory and Critical Care Medicine, 161(2), 381-390. 3,926 smokers with mild-to-moderate airway obstruction (mean age 48.5) randomized to two cessation programs or no intervention; lung function measured yearly for 5 years. Quitters' FEV1 improved by an average of 47 mL (2%) in the year after quitting; afterwards sustained quitters declined 31 mL/year versus 62 mL/year in continuing smokers, comparable to never-smokers. The quitter-versus-smoker comparison is by actual smoking status, not by randomized arm; benefit held despite heavy past smoking, older age or poor baseline function (abstract, PMID 10673175). 10.1164/ajrccm.161.2.9901044
16. Duncan, M. S., Freiberg, M. S., Greevy, R. A., Jr., Kundu, S., Vasan, R. S., & Tindle, H. A. (2019). Association of smoking cessation with subsequent risk of cardiovascular disease. JAMA, 322(7), 642-650. Framingham original and offspring cohorts, 8,770 people, median follow-up 26.4 years; primary analysis in heavy ever smokers (20+ pack-years). Versus current smoking, quitting within 5 years was associated with a lower CVD rate (6.94 vs 11.56 per 1,000 person-years; HR 0.61, 0.49-0.76). The other half: versus never smokers, former smokers' risk stayed significantly elevated beyond 5 years and ceased to be significant only 10 to 15 years after quitting. Observational (abstract, PMID 31429895). 10.1001/jama.2019.10298
17. Morice, A. H., Millqvist, E., Bieksiene, K., Birring, S. S., Dicpinigaitis, P., Domingo Ribas, C., Hilton Boon, M., Kantar, A., Lai, K., McGarvey, L., Rigau, D., Satia, I., Smith, J., Song, W.-J., Tonia, T., van den Berg, J. W. K., van Manen, M. J. G., & Zacharasiewicz, A. (2020). ERS guidelines on the diagnosis and treatment of chronic cough in adults and children. European Respiratory Journal, 55(1), 1901136. Chronic cough: over 8 weeks in adults, 4 weeks in children; global adult prevalence about 10% (meta-analysis). Cough is a vagal reflex; a poor cough reflex leads to recurrent aspiration; polymodal receptors such as TRPV1, TRPA1 and P2X3 on airway nerve endings respond to gastric fluid, acid, smoke, particulates and hyper- or hypotonicity, and ATP from stressed cells is an important stimulus; receptive fields also in lung parenchyma, pharynx, oesophagus and the ear canal (Arnold's reflex); cortical influences modulate the reflex and women have a greater somatosensory cortical area devoted to cough; the system shows redundancy, plasticity and adaptation; most patients show cough reflex hypersensitivity, triggered by low-level stimuli such as cold air, perfumes, smoke and bleach; specialist-clinic patients two-thirds female, most often in their sixth decade. T2 (eosinophilic) inflammation in about a quarter (cough variant asthma, eosinophilic bronchitis). Non-acid and gaseous reflux may contribute and oesophageal dysmotility is highly prevalent in chronic cough. ACE inhibitor cough in about 15%; ACE inhibitors reset the reflex so timing may not match; angiotensin II antagonists do not affect the cough reflex; no patient with cough should be given an ACE inhibitor; bisphosphonates and calcium channel antagonists may worsen reflux and cough; prostanoid eye drops such as latanoprost may descend the lacrimal duct and irritate the pharynx. Smoking is the major remediable cause; smokers have suppressed capsaicin cough sensitivity and cough may transiently increase in the first month after quitting. Stress urinary incontinence, interference with speech and depression are the most impactful complications; women with cough and incontinence have worse quality of life, and incontinence is rarely discussed, so it should be asked about. Initial assessment excludes malignancy, infection, foreign body and ACE inhibitor use; spirometry and chest X-ray; routine chest CT not suggested when X-ray and examination are normal (conditional, very low). Treatment is by sequential therapeutic trials, one agent at a time, stopped if no response; morphine responds within a week, ICS may take a month; if successful continue several months to let neuronal hypersensitivity resolve, then withdraw to test for remission. Short ICS trial 2-4 weeks (conditional, low): of ten RCTs, two in unselected chronic cough found benefit, while in non-asthmatic cough (negative methacholine) ICS was not superior to placebo. Short anti-leukotriene trial 2-4 weeks, particularly in asthmatic cough (conditional, low). Anti-acid drugs not routinely (conditional, low): no benefit over placebo without acid reflux, modest at most with it; high-dose esomeprazole for 12 weeks in patients with rare or no heartburn gave no benefit. Low-dose morphine in refractory cough (strong, moderate); gabapentin or pregabalin (conditional, low), limited by side effects such as dizziness, fatigue, cognitive changes, nausea and blurred vision; cough control therapy (physiotherapy, speech and language therapy) suggested (conditional, moderate). Children: differences in airway morphology, vulnerability, cough-reflex control and immune maturation make cough a symptom of an underlying disease; sudden cough in a healthy preschool child may be foreign-body aspiration requiring bronchoscopy; protracted bacterial bronchitis, a previously unrecognised common cause of wet cough, is defined by continuous wet cough over 4 weeks, no other pointers, and resolution after 2-4 weeks of an appropriate oral antibiotic, and may precede bronchiectasis; neuromodulators not used in children (full text PMC6942543; PMID 31515408). 10.1183/13993003.01136-2019
18. US Preventive Services Task Force (Krist, A. H., Davidson, K. W., Mangione, C. M., et al.). (2021). Interventions for tobacco smoking cessation in adults, including pregnant persons: US Preventive Services Task Force recommendation statement. JAMA, 325(3), 265-279. High certainty that behavioral interventions and FDA-approved pharmacotherapy, alone or combined, give a substantial net benefit for smoking cessation in nonpregnant adults (A recommendation: ask all adults about tobacco use, advise them to stop, provide behavioral interventions and FDA-approved pharmacotherapy). Pregnant persons: behavioral interventions (A); pharmacotherapy evidence insufficient (I). E-cigarettes for cessation: evidence insufficient (I). 14.0% of US adults smoked cigarettes (abstract, PMID 33464343). 10.1001/jama.2020.25019
19. NHS. (2026). Heart attack: symptoms. Symptoms can include chest pain that may feel like crushing or squeezing on the chest and may spread to the arm, neck and jaw; feeling short of breath; feeling or being sick; feeling like indigestion; sweating; and pale, blue or grey skin. Call 999 for chest pain that feels tight or like squeezing, or that spreads to the arms, neck or jaw, with severe difficulty breathing, or if someone becomes unresponsive. A heart attack needs emergency treatment in hospital (page last reviewed 31 March 2026). www.nhs.uk/conditions/heart-attack/symptoms
20. NHS. (2026). Lung cancer: symptoms. Main symptoms include a cough that is not going away, shortness of breath, coughing up blood, chest or shoulder pain, repeated chest infections, unexplained weight loss, loss of appetite and tiredness. See a GP if you've had a cough for longer than 3 weeks or have any other symptoms; ask for an urgent GP appointment or contact NHS 111 if you've coughed up blood or noticed blood on a tissue you've coughed into; call 999 or go to A&E if you're struggling to breathe or have pain in your chest or upper back. These symptoms are often caused by other conditions (page last reviewed 20 August 2026). www.nhs.uk/conditions/lung-cancer/symptoms
21. Hamilton, W., Peters, T. J., Round, A., & Sharp, D. (2005). What are the clinical features of lung cancer before the diagnosis is made? A population based case-control study. Thorax, 60(12), 1059-1065. 247 lung cancers in people over 40 and 1,235 controls matched by age, sex and practice in all 21 Exeter general practices; the whole primary care record for 2 years before diagnosis was coded. Haemoptysis, weight loss, loss of appetite, dyspnoea, chest pain, fatigue and cough, finger clubbing, thrombocytosis and abnormal spirometry were independently associated with lung cancer, as was smoking; excluding the final 180 days before diagnosis, haemoptysis, dyspnoea and abnormal spirometry remained associated (abstract, PMID 16227326). 10.1136/thx.2005.045880