📚 Harmful Components of Tobacco Smoke and Their Effects | 烟草烟雾中的有害成分及其作用
Tobacco smoke is a dynamic aerosol containing over 7,000 chemical substances produced by the incomplete combustion of tobacco leaf and its additives. At least 70 of these are known, probable or possible carcinogens. Understanding the identity and biological action of these components is essential for A-Level Biology, particularly for the chapters on the respiratory and cardiovascular systems.
烟草烟雾是由烟叶及其添加物不完全燃烧产生的一种复杂气溶胶，含有超过 7000 种化学物质，其中至少 70 种为已知、可能或可疑致癌物。理解这些成分的化学属性及其生物学作用对 A-Level 生物考试至关重要，尤其是在呼吸系统与心血管系统相关章节中。
1. The Composition of Tobacco Smoke | 烟草烟雾的组成
Tobacco smoke is divided into two phases. The particulate phase is collected as 'tar' and contains nicotine, polycyclic aromatic hydrocarbons (PAHs), phenol and heavy metals such as cadmium and lead. The gas phase contains carbon monoxide, hydrogen cyanide, nitrogen oxides, formaldehyde and acrolein.
烟草烟雾分为两相：颗粒相被收集为“焦油”，含有尼古丁、多环芳烃（PAHs）、苯酚以及镉、铅等重金属；气相含有一氧化碳、氰化氢、氮氧化物、甲醛和丙烯醛等。
The table below summarises the major components and their key effects, which are frequently tested in CIE examination questions.
下表总结了主要成分及其关键作用，这些内容在 CIE 考试题目中经常出现。
| Component 成分 | Key property 关键特性 | Main biological effect 主要生物学作用 |
|---|---|---|
| Tar, e.g. benzo[a]pyrene 焦油（如苯并芘） | Sticky; contains PAHs 粘稠，含多环芳烃 | Carcinogenesis; paralysis of cilia 致癌；麻痹纤毛 |
| Nicotine C₁₀H₁₄N₂ 尼古丁 | Addictive alkaloid 成瘾性生物碱 | Releases adrenaline; raises heart rate and blood pressure 释放肾上腺素；加快心率、升高血压 |
| Carbon monoxide (CO) 一氧化碳 | Binds haemoglobin about 200× more strongly than O₂ 与血红蛋白的结合力约为 O₂ 的 200 倍 | Forms carboxyhaemoglobin; tissue hypoxia 形成碳氧血红蛋白；组织缺氧 |
| Hydrogen cyanide (HCN) 氰化氢 | Cytotoxic gas 细胞毒性气体 | Damages cilia; inhibits cytochrome oxidase 损伤纤毛；抑制细胞色素氧化酶 |
| Particulates (PM₂.₅) 颗粒物 | Fine solid particles 细小固体颗粒 | Irritate airways; carry carcinogens 刺激气道；携带致癌物 |
2. Tar: A Cocktail of Carcinogens | 焦油：致癌物的“鸡尾酒”
Tar is a sticky brown mixture of thousands of chemicals, including PAHs such as benzo[a]pyrene, N-nitrosamines, aromatic amines and inorganic heavy metals. When smoke is inhaled, the tar condenses on the surfaces of the airways and alveoli, especially at the bifurcations of the bronchi where airflow is turbulent.
焦油是数千种化学物质组成的粘稠棕色混合物，包括苯并芘等多环芳烃、N-亚硝胺、芳香胺和无机重金属。烟雾被吸入后，焦油凝结在气道和肺泡表面，尤其是在支气管分叉处（气流湍急）沉积。
se substitutions, often G→T transversions, particularly in the tumour-suppressor gene p53.
苯并芘本身是一种前致癌物（procarcinogen），需要经肺上皮细胞滑面内质网中的细胞色素 P450 酶活化，生成具有反应活性的环氧化物。该环氧化物与 DNA 中的鸟嘌呤碱基共价结合形成 DNA 加合物，引起碱基替换（常为 G→T 颠换），尤其发生在抑癌基因 p53 中。
If the DNA damage is not repaired by nucleotide excision repair, the mutations accumulate. The combined activation of proto-oncogenes (such as ras and myc) and inactivation of tumour-suppressor genes (such as p53) drives the multistep progression from hyperplasia, through metaplasia and dysplasia, to invasive carcinoma.
如果这些 DNA 损伤未被核苷酸切除修复系统修复，突变就会累积。原癌基因（如 ras、myc）的激活与抑癌基因（如 p53）的失活共同驱动从增生、化生、异型增生到浸润癌的多步骤演进过程。
3. Nicotine: The Addictive Stimulant | 尼古丁：成瘾性兴奋剂
Nicotine (C₁₀H₁₄N₂) is the principal addictive alkaloid in tobacco. It is absorbed rapidly across the alveolar and oral mucosa and reaches the brain within about 10 seconds of inhalation. In the brain, nicotine binds to nicotinic acetylcholine receptors on dopaminergic neurones of the ventral tegmental area, causing release of dopamine in the nucleus accumbens, which produces pleasure and reinforces smoking behaviour.
尼古丁（C₁₀H₁₄N₂）是烟草中主要的成瘾性生物碱。它能快速穿过肺泡黏膜和口腔黏膜，吸入后约 10 秒内到达大脑。在大脑中，尼古丁结合中脑腹侧被盖区多巴胺能神经元上的烟碱型乙酰胆碱受体，促使伏隔核释放多巴胺，产生愉悦感并强化吸烟行为。
Nicotine also stimulates nicotinic receptors at autonomic ganglia and on the chromaffin cells of the adrenal medulla. This triggers the release of adrenaline and noradrenaline into the circulation, producing sympathetic effects: increased heart rate, increased stroke volume, raised blood pressure and constriction of peripheral arterioles.
尼古丁还会刺激自主神经节和肾上腺髓质嗜铬细胞上的烟碱型受体，促使肾上腺素和去甲肾上腺素释放入血，产生交感效应：心率加快、每搏输出量增加、血压升高以及外周小动脉收缩。
In addition, nicotine increases platelet adhesiveness and raises plasma fibrinogen concentration. These changes promote thrombus formation and accelerate the development of atherosclerosis, explaining why smokers have a 2-4 times higher risk of coronary heart disease and stroke.
此外，尼古丁增加血小板黏附性并升高血浆纤维蛋白原浓度。这些变化促进血栓形成并加速动脉粥样硬化的发展，这就解释了吸烟者患冠心病和中风的风险为何升高 2-4 倍。
4. Carbon Monoxide: The Silent Suffocator | 一氧化碳：沉默的“窒息者”
Carbon monoxide (CO) is a colourless, odourless gas produced by incomplete combustion of tobacco. It competes with oxygen for the oxygen-binding sites on haemoglobin. Because CO binds to haemoglobin approximately 200-250 times more strongly than O₂, even a small concentration of CO in inspired air dramatically reduces the oxygen-carrying capacity of the blood.
一氧化碳（CO）是烟草不完全燃烧产生的无色无味气体。它与氧气竞争血红蛋白上的氧结合位点。由于 CO 与血红蛋白的结合力约为 O₂ 的 200-250 倍，即使吸入气中 CO 浓度很低，也会显著降低血液的携氧能力。
The product, carboxyhaemoglobin (HbCO), cannot transport oxygen. In a heavy smoker, up to 10-15% of haemoglobin may be bound to CO, so the same blood flow delivers much less oxygen to tissues. CO also shifts the oxygen dissociation curve of the remaining oxyhaemoglobin to the left, which means that haemoglobin binds O₂ more avidly and releases less O₂ to the tissues at any given partial pressure.
产物碳氧血红蛋白（HbCO）无法运输氧气。重度吸烟者体内多达 10-15% 的血红蛋白与 CO 结合，因此相同的血流向组织输送的氧气大大减少。CO 还会使剩余氧合血红蛋白的氧解离曲线左移，这意味着在任何给定氧分压下，血红蛋白结合 O₂ 更牢固，向组织释放的 O₂ 更少。
This tissue hypoxia has serious consequences. The heart must work harder to deliver oxygen, increasing myocardial workload and precipitating angina in people with narrowed coronary arteries. In pregnant women, CO crosses the placenta and reduces oxygen delivery to the fetus, contributing to fetal growth restriction and low birth weight.
这种组织缺氧后果严重。心脏必须更努力地输送氧气，加重心肌负荷，并可在冠状动脉狭窄的患者中诱发心绞痛。在孕妇中，CO 透过胎盘减少胎儿供氧，导致胎儿生长受限和低出生体重。
5. Irritant Gases and Particulates | 刺激性气体与颗粒物
Each cigarette generates billions of fine particles, most in the PM₂.₅ size range (diameter below 2.5 μm). These particles penetrate deep into the terminal bronchioles and alveoli, carrying adsorbed carcinogens on their large surface area. They activate alveolar macrophages and epithelial cells to release pro-inflammatory cytokines such as tumour necrosis factor-α and interleukins.
每支香烟产生数十亿颗细小颗粒，多数属于 PM₂.₅ 范围（直径小于 2.5 μm）。这些颗粒能够深入终末细支气管和肺泡，并借助巨大的比表面积携带吸附的致癌物。它们激活肺泡巨噬细胞和上皮细胞，释放肿瘤坏死因子-α、白介素等促炎细胞因子。
Hydrogen cyanide is another gas-phase component that specifically paralyses ciliary beating by inhibiting the enzyme cytochrome oxidase in the mitochondria of ciliated cells. Nitrogen oxides and acrolein react with water in the airway lining to form free radicals and reactive oxygen species (ROS), which deplete antioxidants such as glutathione and cause oxidative damage to lipids, proteins and DNA.
气相中的氰化氢通过抑制纤毛细胞线粒体内的细胞色素氧化酶，特异性地麻痹纤毛运动。氮氧化物和丙烯醛与气道内衬液中的水反应，产生自由基和活性氧（ROS），耗竭谷胱甘肽等抗氧化剂，造成脂质、蛋白质和 DNA 的氧化损伤。
Together, the irritant gases and particles produce airway inflammation, oedema, increased mucus secretion and reflex bronchoconstriction. This is why smokers often experience a persistent cough and wheeze even before chronic disease is diagnosed.
刺激性气体和颗粒物共同引起气道炎症、水肿、黏液分泌增加和反射性支气管收缩。这就是为什么吸烟者在慢性疾病确诊之前就常有持续咳嗽和喘息的原因。
6. Destruction of the Mucociliary Clearance System | 黏液纤毛清除系统的破坏
In healthy airways, a mucociliary escalator removes inhaled debris and pathogens. Goblet cells and submucosal glands secrete a layer of mucus, while the coordinated beating of cilia on ciliated epithelial cells moves the mucus upwards towards the pharynx, where it is swallowed. This system continuously cleans the respiratory surface.
在健康气道中，“黏液纤毛传送带”负责清除吸入的碎屑和病原体。杯状细胞和黏膜下腺体分泌一层黏液，同时纤毛上皮细胞上纤毛的协调摆动将黏液向上推向咽部并被吞咽，从而持续清洁呼吸表面。
Tar and hydrogen cyanide paralyse and eventually destroy the cilia, while chronic inflammation causes goblet-cell hyperplasia and submucosal gland hypertrophy, leading to excessive mucus production. The airway epithelium also undergoes squamous metaplasia: the normal columnar ciliated cells are replaced by stratified squamous cells that lack cilia.
焦油和氰化氢麻痹并最终破坏纤毛，而慢性炎症导致杯状细胞增生和黏膜下腺体肥大，黏液分泌过多。气道上皮还发生鳞状化生：正常柱状纤毛细胞被缺乏纤毛的复层鳞状细胞取代。
The result is that mucus and trapped pathogens cannot be removed efficiently. They pool in the smaller airways, producing 'smoker's cough' and creating a favourable environment for bacterial and viral infections. The loss of this defence mechanism is one of the earliest measurable changes in smoking-related lung disease.
其结果是黏液和被捕获的病原体无法被有效清除，在小气道中积聚，产生“吸烟者咳嗽”并为细菌和病毒感染创造了有利环境。这种防御机制的丧失是吸烟相关肺病中最早可测到的变化之一。
7. Chronic Bronchitis | 慢性支气管炎
Chronic bronchitis is clinically defined as a persistent cough with sputum production on most days for at least three months of the year, in two consecutive years. It is caused by long-term irritation of the large airways by tobacco smoke. Post-mortem and biopsy studies show submucosal gland enlargement, goblet-cell hyperplasia and a heavy inflammatory infiltrate of neutrophils and macrophages.
慢性支气管炎的临床定义为连续两年中每年至少三个月、大多数日子出现咳嗽并咳痰。它由烟草烟雾对大气的长期刺激引起。尸检和活检研究显示黏膜下腺体增大、杯状细胞增生以及大量中性粒细胞和巨噬细胞炎性浸润。
The excess mucus narrows the airway lumen, while inflammation thickens the bronchial wall. Airway resistance therefore rises, and the patient experiences breathlessness, wheezing and frequent chest infections. Because the damage is chronic and progressive, the airflow limitation becomes only partially reversible.
过多的黏液使气道管腔变窄，炎症则使支气管壁增厚。因此气道阻力升高，患者出现呼吸困难、喘息和频繁的胸部感染。由于损伤是慢性且进行性的，气流受限只能被部分逆转。
8. Emphysema and COPD | 肺气肿与慢性阻塞性肺疾病
Emphysema is defined anatomically as permanent enlargement of the air spaces distal to the terminal bronchiole, with destruction of the alveolar walls. In response to smoke particles, alveolar macrophages release chemotactic factors that recruit neutrophils. Both cell types release the proteolytic enzyme elastase, which digests elastin and other components of the alveolar extracellular matrix.
肺气肿的解剖学定义是终末细支气管以远的肺泡腔永久性扩大，并伴有肺泡壁破坏。烟雾颗粒激活肺泡巨噬细胞释放趋化因子，招募中性粒细胞。这两类细胞均释放蛋白水解酶弹性蛋白酶（elastase），分解肺泡细胞外基质中的弹性蛋白及其他成分。
Healthy lungs are protected by α₁-antitrypsin, a serum protease inhibitor that neutralises elastase. Reactive oxygen species in cigarette smoke oxidise and inactivate α₁-antitrypsin, tipping the balance towards proteolysis. Smoke also directly damages alveolar epithelial cells, and the resulting chronic inflammation accelerates the destruction.
健康肺依靠血清蛋白酶抑制剂 α₁-抗胰蛋白酶来中和弹性蛋白酶。香烟烟雾中的活性氧会氧化并使 α₁-抗胰蛋白酶失活，从而使平衡偏向蛋白水解。烟雾还直接损伤肺泡上皮细胞，慢性炎症进一步加速破坏过程。
The loss of alveolar walls has two major consequences. First, the surface area available for gas exchange is greatly reduced, causing hypoxia and hypercapnia. Second, the destruction of elastic tissue removes the lung's elastic recoil, so small airways collapse during expiration, trapping air and producing the hyperinflated 'barrel chest' typical of emphysema. Chronic bronchitis and emphysema together form chronic obstructive pulmonary disease (COPD), which is irreversible and progressive.
肺泡壁的丧失带来两大后果：第一，可用于气体交换的表面积大幅减少，造成低氧血症和高碳酸血症；第二，弹性组织破坏使肺失去弹性回缩力，小气道在呼气时塌陷、气体潴留，产生肺气肿典型的过度充气“桶状胸”。慢性支气管炎与肺气肿合称慢性阻塞性肺疾病（COPD），不可逆且呈进行性发展。
9. Lung Cancer | 肺癌
Smoking is the single largest cause of lung cancer, accounting for about 85-90% of cases. The risk is directly proportional to both the number of cigarettes smoked per day and the duration of smoking. Squamous cell carcinoma and small-cell carcinoma are the two types most strongly associated with tobacco use, because they arise from the metaplastic squamous epithelium and neuroendocrine cells that proliferate in response to smoke.
吸烟是肺癌的最大单一诱因，约占病例的 85-90%。风险与每日吸烟支数和吸烟年限成正比。鳞状细胞癌和小细胞癌是与吸烟关系最密切的两种类型，因为它们起源于对烟雾产生化生反应的鳞状上皮和增殖的神经内分泌细胞。
nitrosamines into DNA-reactive intermediates. These form adducts that cause miscoding mutations. Mutational 'hotspots' ns inactivate the gene and allow damaged cells to escape apoptosis and cell-cycle control.
其分子机制始于多环芳烃和亚硝胺被代谢活化为可与 DNA 反应的中间产物。它们形成加合物并引起错误编码突变。突变“热点”位于 p53 抑癌基因中，G→T 颠换使该基因失活，受损细胞因此逃脱凋亡和细胞周期监控。
Mutations in the K-ras proto-oncogene are also common and result in constitutive activation of cell signalling pathways that drive uncontrolled proliferation. Because lung cancer is usually diagnosed late, the five-year survival rate remains below 20%, making prevention by smoking cessation the most effective public health intervention.
K-ras 原癌基因突变也很常见，导致驱动细胞不受控增殖的信号通路持续激活。由于肺癌通常发现较晚，五年生存率仍低于 20%，因此通过戒烟进行预防是最有效的公共卫生干预手段。
10. Effects on the Cardiovascular System | 对心血管系统的影响
The cardiovascular system is attacked by tobacco smoke through three parallel mechanisms. First, nicotine raises heart rate, cardiac output and blood pressure through adrenaline release, increasing the workload on the left ventricle. Second, carbon monoxide reduces oxygen delivery to the myocardium, so the heart is forced to work harder with less oxygen.
心血管系统受到烟草烟雾三条平行途径的攻击。第一，尼古丁通过肾上腺素释放加快心率、增加心输出量和升高血压，加重左心室负荷。第二，一氧化碳减少心肌的氧供，迫使心脏在缺氧状态下更费力地工作。
Third, free radicals in smoke damage the vascular endothelium, exposing the underlying tissue and allowing LDL cholesterol to accumulate in the arterial wall. Platelets activated by nicotine become stickier and aggregate on the injured surface, initiating the formation of an atheromatous plaque. Over time, plaques narrow the coronary arteries and may rupture, causing thrombosis, myocardial infarction and stroke.
第三，烟雾中的自由基损伤血管内皮，暴露内皮下组织，使 LDL 胆固醇沉积
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