عدد الرسائل : 195
العمر : 47
تاريخ التسجيل : 27/07/2008
|موضوع: smoking & air pollution السبت أغسطس 02, 2008 3:49 am|| |
SMOKING AND AIR POLLUTION
General household surveys in the UK showed a decline in the prevalence of cigarette smoking in the early nineties. More recent data show that this decline has halted and smoking in the UK is on the increase. At present, 28% of men and women aged 16 years and over smoke. Cigarette smoking is most common between the ages of 16 and 34 years (40% in both sexes) and it is in this age group that the increase has occurred. At the age of 15 more girls (33%) than boys (13%) smoke cigarettes. A greater proportion of manual workers than professional workers smoke. In the USA only 26% of men smoke and 22% of women. However, cigarette consumption is rising in Central and Eastern Europe and many developing countries including China.
Cigarette smoke contains polycyclic aromatic hydrocarbons and nitrosamines, which are potent carcinogens and mutagens in animals. It causes release of enzymes from neutrophil granulocytes and macrophages that are capable of destroying elastin and leading to lung damage. Pulmonary epithelial permeability increases even in symptomless cigarette smokers, and correlates with the concentration of carboxyhaemoglobin in blood. This altered permeability possibly allows easier access to carcinogens.
Cigarette smoking is addictive. People usually start smoking in adolescence for psychosocial reasons and, once it is a regular habit, the pharmacological properties of nicotine play a major part in persistence, conferring some advantage to the smoker's mood. Very few cigarette smokers (less than 2%) can limit themselves to occasional or intermittent smoking. The dangers are listed in Table 14.6.
Table 14-6. The dangers of cigarette smoking
Carcinoma of the oesophagus
Ischaemic heart disease
Peripheral vascular disease
An increase in abnormal spermatozoa
A decrease in birthweight of the infant
An increase in fetal and neonatal mortality
An increase in asthma
Risk of asthma, pneumonia and bronchitis in infants of smoking parents
An increase in cough and breathlessness in smokers and non-smokers with COPD and asthma
Increased cancer risk
Table 14-7. Effects of smoking on the lung
Large airways Small airways
Increase in submucosal gland volume Increase in number and distribution of goblet cells
Increase in number of goblet cells Airway inflammation and fibrosis
Chronic inflammation Epithelial metaplasia/dysplasia
Metaplasia and dysplasia of the surface epithelium Carcinoma
Proximal acinar scarring
Increase in alveolar macrophage numbers
Emphysema (centriacinar, pan-acinar)
There is a significant dose-response relationship between the smoking of 0-40 cigarettes daily and lung cancer mortality (Table 14.7). Sputum production and airflow limitation increase with daily cigarette consumption, and effort tolerance decreases, partly owing to high levels of carboxyhaemoglobin in bronchitis patients. Smoking and asbestos exposure are synergistic in producing bronchial carcinoma, increasing the risk in asbestos workers by up to five to eight times that of non-smokers exposed to asbestos.
Cigarette smokers who change to other forms of tobacco can reduce the risk, even if they continue to inhale, and are better off changing to cigars or pipes. However, all pipe and cigar smokers also have a greater risk of lung cancer than lifelong non-smokers or former smokers.
Environmental tobacco smoke ('passive smoking') has been shown to cause more frequent and more severe attacks of asthma in children and possibly increases the number of cases of asthma. It is also associated with a small but definite increase in lung cancer.
If the entire population could be persuaded to stop smoking, the effect on healthcare use would be enormous. National campaigns, bans on advertising and a substantial increase in the cost of cigarettes are the best ways of achieving this at the population level. Meanwhile, active encouragement to stop smoking remains a useful approach for individuals. Smokers who want to stop should have access to smoking cessation clinics to provide behavioural support. Nicotine replacement therapy (NRT) and buproprion are effective aids to smoking cessation in those smoking more than 10 cigarettes per day. Both should only be used in smokers who commit to a target stop date, and the initial prescription should be for 2 weeks beyond the target stop date. NRT is the preferred choice; there is no evidence that combined therapy offers any advantage. Therapy should be changed after 3 months if abstinence is not achieved.
Atmospheric air pollution, due to the burning of coal for energy and heat, has been a characteristic of urban living in developed countries for at least two centuries. It consists of black smoke and sulphur dioxide (SO2). Air pollution of this type peaked in the 1950s in the UK, until legislation led to restrictions on coal burning. Such pollution continues to increase in newly industrialized countries (India, China) and continues in Eastern Europe and Russia. The combustion of petroleum and diesel oil in motor vehicles has led to new air pollution, consisting of primary pollutants such as the oxides of nitrogen (NO and NO2), diesel particulates, polyaromatic hydrocarbons and the secondary pollutant ozone (O3) generated by photochemical reactions in the atmosphere. Levels of NO2 can be higher in poorly ventilated kitchens and living rooms where gas is used for cooking and in fires. In Europe 70% of the particulates present in urban air result from the combustion of diesel fuel. Very small particles (<2.5 μm, particulate matter PM2.5) remain airborne for long periods and are carried into rural areas. In the UK, ozone concentrations are highest in sunny rural areas.
Classical studies in the 1950s showed that winter-time episodes of severe air pollution (smog) were associated with substantial numbers of deaths from respiratory disease, particularly when temperature inversion trapped black smoke and SO2 over urban areas. Air pollution of this type continues to cause excess deaths from respiratory and cardiovascular disease in older populations, and symptoms of bronchitis in children. Pollution resulting primarily from motor vehicles has been shown to cause:
Increased deaths from respiratory and cardiovascular causes in the elderly - particulates less than 10 μm in diameter (PM10).
Increased respiratory symptoms, hospital admissions and reduced lung function in children and younger adults - SO2, NO2, O3, PM10. Frequently there is a lag of 1-2 days between peaks in air pollution and disease effects.
Increase in lung cancer - polyaromatic hydrocarbons.
It has been proposed at various times that air pollution is one of the causes of the dramatic increase in asthma and other allergic diseases (Table 14.8). There is no current evidence that this is true, but both NO2 and ozone have been shown to enhance the nasal and lung airway responses to inhaled allergen, in those with established allergic disease. Air pollution has, however, been shown to have an adverse effect on lung development in teenage children.
Asthmatics are advised to avoid exercising outdoors when air quality is poor and to increase their anti-inflammatory medication (i.e. inhaled corticosteroids).
Short- and long-term measures are required to reduce air pollution, particularly diesel particulates (which are predicted to increase as more diesel engines are used). Such measures include increased motor engine efficiency, catalytic converters, diesel particulate traps, and decreased reliance on cars and trucks.
Table 14-8. Air pollutants and their health effects
Average concentration Poor air quality Susceptible individuals Mechanisms of health effects
Sulphur dioxide (SO2) 5-15 ppb > 125 ppb Asthmatics Bronchoconstriction through neurogenic mechanism
Ozone (O3) 10-30 ppb > 90 ppb All affected, particularly during exercise Restrictive lung defect
Enhanced response to allergen
Nitrogen dioxide (NO2) 25-40 ppb > 100 ppb Allergic individuals Airway inflammation Enhanced response to allergen
Particulate matter (PM10) 25-30 μg/m3 > 70 μg/m3 Elderly
Allergic individuals Airway and alveolar inflammation
Enhanced production selectively of the allergy antibody (IgE)
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