Cigarette smoking is also firmly established as a major risk factor for COPD (Table 1). Data from longitudinal, crosssectional, and case-control studies show that in comparison with nonsmokers, cigarette smokers have higher death rates for chronic bronchitis and emphysema; higher prevalence and incidence rates for chronic bronchitis, emphysema, and obstructive airways disease; and higher frequencies of respiratory symptoms and lung function abnormalities. They also have a greater average annual rate of decline in FEVvDifferences between cigarette smokers and nonsmokers increase as cigarette consumption increases. Pipe and cigar smokers have higher morbidity and mortality rates for COPD than nonsmokers, but lower rates than cigarette smokers.
There is also ample evidence to show that stopping smoking is beneficial. Ibe prevalence of symptoms, chest illnesses, and disease is generally less in exsmokers than in continuing smokers, and levels of lung function are higher and rates of decline lower in exsmokers than continuing smokers. However, it appears that lost lung function is not regained. Length of time since stopping, age at stopping, amount smoked, and stage of disease at time of stopping all influence the outcome. As might be expected, exsmokers resemble nonsmokers more closely when they give up smoking at an early age or after a short period of smoking only a few cigarettes. Prognosis is less hopeful if cessation occurs at older ages, among heavy smokers, and if disease is already advanced.
Although the importance of cigarette smoking as a cause of COPD is firmly established, some facets of the problem are not fully understood. For example, the health effects of cigarette smoking are not of equal frequency or severity in all smokers. Cigarette smoke does not act in isolation on uniformly susceptible people, but rather in a variable context in which personal factors and exposures to other environmental hazards, as well as the composition and dose of cigarette smoke, influence the onset and course of disease.
Cigarettes in current use differ substantially from cigarettes in use at the start of the epidemiologic studies which implicated smoking as a health hazard. The tar and nicotine contents of sales-weighted average cigarettes are now less than half their former levels, and other changes in the quality and character of cigarette smoke have resulted from the use of filters, changes in tobacco and manufacturing processes, and use of new natural and synthetic products. Current smokers also differ in several ways from smokers of 20 years ago; eg, a higher proportion are women, and the percentage of smokers smoking 25 or more cigarettes a day has increased. A lot of diseases may be caused by smoking that’s why My Canadian Pharmacy starts solving this problem due to the remedies of our pharmacy.
Ibe health effects of cigarettes on the market today are uncertain. Recent evidence indicates that low-nicotine cigarettes do not deliver a lower dose of nicotine to smokers, and one study showed that tar content of cigarettes was unrelated to pulmonary (unction at baseline or 5 years later, although there was a significant relationship between the number of cigarettes smoked per day and FEV and FVC. Effects of involuntary exposure to cigarette smoke have also attracted attention recently. Mean levels of ventilatory lung function (read also Lung Cancer) are significantly lower and prevalence rates of respiratory symptoms and diseases higher in nonsmoking wives of smoking husbands, and in nonsmoking children of smoking parents. Although the effect of passive smoking appears to be small, it is important because of the frequency and involuntary nature of the exposure.
Reduced Lung Function
People with obstructive airways disease (OAD) may have experienced excessive decline in lung function from levels which were previously normal, or they may have started out with levels at the low end of the normal range and experienced average declines with age. The former pattern has been referred to as the horse-racing effect. The latter pattern, known as tracking, is a situation in which individuals tend to maintain their relative position or rank in the distribution over a period of time. In practice, both phenomena are probably important, and a combination of excessive decline plus low normal lung function to start with will obviously result in clinical impairment at a relatively young age. Incidence rates of obstructive airways disease were related inversely to initial levels of FEV, FVC, and FEFW in 10- and 15-year follow-up studies of the population ofTecum-seh (see below).’ Incidence rates were also related to other indices of lung function, such as the nitrogen index of uneven ventilation. In men but not in women, incidence rates of OAD were significantly higher in those who had the biggest increase in FEV or FVC after inhalation of isoproterenol.
Death rates for chronic respiratory diseases are higher than expected among men in certain occupations and industries. Standardized mortality ratios (SMRs) were published for 1950 in the United States, and in these and more recent data for England and Wales, ratios were high for workers in coal and other types of mining and quarrying, metal molding, manufacture of stone, glass, and clay products, and in laborers. Epidemiologic surveys have shown that work in cotton, flax, hemp, or grain dust; fire-fighting; and work involving exposure to asbestos or coke oven emissions is associated with respiratory symptoms and/or reduced lung function. Inception rates for chronic bronchitis were high in the United Kingdom for miners and quarry men, laborers, drivers of stationary engines, furnace, forge, foundry and rolling mill workers, as well as for men who worked with gas, coke, or chemicals, or who were glass or ceramic makers. Higher morbidity and mortality rates in these occupations and industries and in blue-collar workers generally are not necessarily due to harmful exposures in the workplace. In the U. K., SMRs for bronchitis tend to be high for wives as well as for the men themselves, which suggests that other factors, such as exposure to general and domestic air pollution and general standard of living, may be involved. In addition, cigarette smoking is more prevalent among blue-collar than white-collar workers. Comparisons of prevalence rates of respiratory symptoms and mean levels ofFEV! in miners and nonminers in West Virginia showed that respiratory function was poorest in miners who smoked and best in nonsmoking nonminers. It is difficult, if not impossible, to attribute nonspecific symptoms or reduced levels of pulmonary function to specific causes or to determine the contribution which each of several factors makes to impairment of the respiratory system. Interaction between cigarette smoking and certain occupational hazards results in increased rates of COPD, and some studies have suggested that exposure to asbestos, cotton dust, and crystalline silica is more harmful to cigarette smokers than to nonsmokers. Relationships between certain occupational exposures and chronic airways obstruction were discussed by Weill at this conference.
Table 1—Risk Factors for COPD
|AgeMale sexCigarette smoking Reduced lung function Occupational exposures Air pollutionо-defident phenotypes (PiZ, PiSZ) Probable and Possible|
|Infections of the respiratory tract Allergic conditions Bronchial reactivity LeannessSocioeconomic circumstances Aloohol intake Diet and nutritionABO, ABH secretor, kell phenotypes Impaired immune defenses Hormonal factors Familial factors Climate|