According to the WHO, in 2001 COPD was the fifth highest cause of death in the world. In epidemiology, distinct phenotypic entities sometimes come under the term COPD, so that prevalence and mortality data are inclusive of chronic bronchitis, emphysema and asthma in an uneven way.
Although COPD and bronchial asthma are characterised by different phatophysiologic mechanisms and cellular patterns, persisting chronic asthma may evolve as an irreversible form of airway obstruction. In that case, asthma must be analysed under within the umbrella of COPD.
A DEADLY DISEASE
According to the data provided by the WHO, in 2001 COPD caused 2,676,000 deaths.
There are considerable differences in COPD mortality rates between countries, which is directly related to the different distributions of tabagism and other risk factors. Remarkable differences are shown even in Europe, where 200,000–300,000 people die each year because of the disease.
According to the WHO, in 1997 COPD was the cause of death for 4.1% of males and 2.4% of females in Europe. Moreover, a COPD mortality increase among females was observed in North European countries from 1980–90. Between 1995 and 1999, smoking caused just under 65,000 deaths by COPD each year in the US adult population. In Italy, about half of the 37,782 deaths caused by respiratory diseases in 2000 were caused by COPD.
In Europe, 4%–6% of the adult population suffers from COPD in a clinically relevant form, although two thirds of it show only minor ventilatory impairments. The prevalence increases proportionally with age. The multicentre European Community Respiratory Health Survey (ECRHS), carried out in 16 nations (with 18,000 subjects aged between 20 and 44 years old), estimated a mean chronic bronchitis prevalence of 2.6%.
The individual and social COPD burden is going to rise during the coming decades, and it will be mainly borne by females, due to previously lower smoking numbers and to the population ageing.
A major problem with COPD is estimating its real prevalence in the general population, which may considerably change according to the diagnostic tools used: respiratory symptoms reported by the patient, physician’s diagnosis or presence of lung-function impairments.
Even when COPD diagnosis is based on an objective verification, such as spirometry, variation inside the same population may be considerable given the different criteria the main international scientific societies use to define bronchial obstruction.
It is obviously necessary to fix a standardised criterion, epidemiologically valid and accepted by all the societies involved in respiratory medicine. Such an objective has not yet been reached, even after the introduction of GOLD criterion on COPD diagnosis, either to give information about prognostic value in patients or to apply it to the whole population, regardless of age.
Another considerable epidemiological aspect is COPD underdiagnosis. In scientific literature, underdiagnosis fluctuates between 25% and 50%, according to considered surveys. It appears that the disease may be more frequent than expected, as about 18% of the investigated subjects reported chronic bronchitis, asthma or emphysema diagnosis, or showed obstructive spirometric findings.
The intuition that many who suffer from COPD do so without being aware of it, thereby delaying the therapeutic treatment and allowing the disease to evolve into severe stages, has driven a few researchers to conceive of early diagnosis studies. For instance, a spirometric screening on smokers could identify subjects with obstructive findings.
Risk factors for developing COPD may be divided into two categories: exogenous and endogenous. Such factors, separately or in synergy, determine the subject’s susceptibility level for the disease growth.
EXOGENEOUS RISK FACTORS
Exogeneous risk factors include tobacco smoke, work exposure, outdoor and indoor pollution, socio-economic conditions and diet.
Tobacco smoke is without any doubt the main risk factor for COPD development and for mortality. In 2000, 4.83 million deaths were attributed to smoking (which accounts for 12% of the total mortality recorded in adults). In industrialised countries, the percentage of COPD deaths due to smoking has been 80.5% in men and 61.5% in women.
Indeed, the fifty-year follow up study by British doctors has shown that about two thirds of smokers die from smoke-related causes and on average ten years younger than non smokers. Moreover, it has been shown that current smokers have a COPD mortality rate 12.7 times higher than non smokers. Such rates rise proportionally to the increasing mean of cigarettes smoked daily.
The starting age, the mean of daily cigarettes and the years spent smoking all contribute in a different way to the origin of the pulmonary damage. Although it is commonly reported in the literature that only 10%–20% of smokers develop the disease, recent epidemiological investigations show that COPD signs / symptoms are present in 40%–50% of smokers.
Chronic exposure to pollutants at work may contribute to COPD development. Workers particularly exposed to this risk belong to metallurgic, mining, building, agricultural, textile, chemical, paper and food industries.
Subjects with work exposure have shown a faster lung function
decline and a higher prevalence for respiratory symptoms and/or chronic diseases. A synergetic effect of tobacco smoking and work exposure has been noted.
Recent articles have shown that population attributable risk due to work exposure is about 15% for chronic bronchitis and 18% for lung function impairments related to COPD.
Conventional outdoor pollutants are fossil fuel smoke, sulphur diotide (SO2), nitrogen oxides (NOx) and ozone (O3) . Chronic exposure to elevated air pollution levels seems to correlate with chronic bronchitis and lung function impairments.
In the last few years, the study of the effects of suspended particulates with aerodynamic diameter <10μm (PM10) or <2.5μm (PM2.5), on deaths caused by cardio-respiratory problems, has created a great deal of interest in the scientific community.
A recent epidemiological survey has shown that each increase of 10μg / m3 in suspended particulates is equivalent to a 6% mortality risk rise.
Across the developed world people spend most of their time in enclosed buildings and are therefore constantly exposed to the highly dangerous effects of indoor pollutants. The indoor pollutants particularly related to COPD development risk are Environmental Tobacco Smoke (ETS), Particulate Matter (PM) and biomass combustion.
Research has shown an evident association between ETS exposure and a reduction of FEV1 physiological growth rate in children. The consequent inadequate respiratory system maturation during childhood may lead to COPD development in adulthood. European studies have shown a clear association between chronic bronchitis and/or COPD diagnosis and ETS exposure in the adult population.
Increases in PM concentration, mainly from inhaling tobacco smoke and combustion processes, have been linked to highly increased respiratory symptom incidence and lung function impairments, both in children and adults.
This term includes indicators, such as education, occupation, home life and income. Several epidemiological studies have pointed out a correlation between socio-economic level and risk of developing COPD.
The role of dietetic habits as a risk factor is the object of much research. In general, antioxidants seem to have preventative proper ties linked to reducing physiological deterioration caused by ageing. Several epidemiological researches have shown that a regular fruit and vegetable consumption is linked to a reduction in the risk of COPD development.
Flavonoids, micronutrients such as magnesium and selenium, omega-3 fatty acids and a moderate alcohol consumption, have been studied for their possible protective action on respiratory system. Excessive alcohol consumption has been associated with a higher COPD prevalence and a faster lung-function decline.
ENDOGENOUS RISK FACTORS
Endrogenous risk factors include genetic factors, gender, childhood respiratory troubles and family history.
It is well known that a genetic Mendelian transmission can induce a serum protease associated with an increased risk of inhibitor deficit-1-antitrypsin pulmonary emphysema of panacinar type in young subjects characterised by a genetic recessive trait (ZZ), the phenotypic expression of which is influenced by smoking. Even the heterozygosity condition for Z allele is considered per se a risk factor for COPD development.
COPD AND GENDER
In many parts of the world COPD prevalence rates are higher among men than women. This is usually attributable to both reduced tobacco smoking prevalence and a reduced work exposure to noxious substances. Really, the recent smoking increase amongst women has been followed by a concomitant increase in COPD prevalence, as
reported, for instance, in the USA.
CHILDHOOD RESPIRATORY TROUBLES
Many epidemiological studies have pointed out the role of respiratory diseases that occur during childhood as an independent risk factor for COPD development.
Lung function impairments have traditionally been associated with familial history. This aggregation, sometimes independent of smoking, may highlight a genetic predisposition to the disease development, which still needs further investigation.
Direct costs include hospital admissions, out-patient visits and domiciliary assistance, as well as pharmacological treatment. Indirect costs are mainly the disease disabling effects, which cause loss of working days.
In the USA, it was estimated in 2000 that COPD cost around $30.4bn. Within the European Community, the annual cost of COPD is about €38.8bn.
The COPD burden for developed countries seems to be considerable, and bound to increase during the coming years. The high prevalence of smokers worldwide below the age of 45 suggests the quality of preventive medical services must be improved, with increased efforts by public health specialists, pneumologists and primary care physicians.