NOT FOR QUOTATION WITHOUT THE PERMISSION OF THE AUTHORS
THE FVTURE
OF LUNGDISEASES:
COPD MODEL FOR SLOVAKIA
M. R u s n a k A. Y a s h i n P. K r i s t q f e k
December 1985 CP-85-49
C o l l a b o r a t i v e P a p e r s r e p o r t work which h a s not been performed solely at t h e International Institute for Applied Systems Analysis and which h a s r e c e i v e d only limited review. Views or opinions e x p r e s s e d h e r e i n d o not necessarily r e p r e s e n t those of t h e Institute, i t s National Member Organizations, or o t h e r organizations supporting t h e work.
INTERNATIONAL INSTITUTE FOR APPLIED SYSTEMS ANALYSIS 2361 Laxenburg, Austria
CONTENTS
Introduction
1. COPD Epidemiology in Some Countries 2. Why COPD Model?
3. Causes and Development of COPD
3.1 Risk F a c t o r s f o r COPD Development 4. COPD Model Objectives
5. COPD Model S t r u c t u r e
5.1 Population Development Prognosis 5.2 COPD Risk F a c t o r s Prognosis 6. COPD Model Realization
6.1 Model Derivation 6.2 Implementation 6.3 Demographic D a t a 6.4 Number of COPD Cases 6.5 Risk of Developing COPD 6.6 Risk F a c t o r s P r e v a l e n c e
6.7 Transition Coefficients Between Groups 7. Results and Discussion
Conclusions References
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THE FUTURE OF LUNG DISEASES:
COPD MODEL
FOR SLOVAKIAM. Rusnak*,
A.
Yashin** andP.
Kristufik***INTRODUCTION
The initial explorations of bronchial t r e e pathology c a n b e t r a c e d back t o t h e e a r l y p a r t of t h e nineteenth century. Laennec w a s t h e f i r s t t o demonstrate t h e so-called " c a t a r r h pulmonaire" and i t s significance t o t h e disease (Ba jan 1983). but t h e attention of physicians c e n t e r e d upon tuberculosis and pneumonia up until t h e 1950s. The death of more t h a n 4000-mainly older-people during a c a t a s t r o p h i c four-day smog in London (1952) and t h e realization t h a t c h r o n i c bronchitis and i t s complications were t h e fatal causes h a s proved t h e importance of studying this group of diseases (Protivinski 1968).
Intensive r e s e a r c h h a s demonstrated t h e necessity f o r a more p r e c i s e defini- tion of t h e group of illnesses d e s c r i b e d under t h e g e n e r a l term c h r o n i c nonspecif- i c lung diseases. Common e f f o r t s of specialists from all o v e r t h e world have cul- minated in a c c e p t e d definitions of chronic bronchitis, pulmonary emphysema and bronchial asthma by t h e World Health Organisation (WHO 1980). Recently, a com- mon term has been used by mostly American a u t h o r s f o r a l l of t h e s e diagnostic un- its: c h r o n i c o b s t r u c t i v e pulmonary disease (COPD).
Numerous studies have shown a n undesirable s p r e a d of COPD in t h e developed countries. The high and still growing prevalence of t h e s e diseases creates a bur- den on health-care systems, which leads t o a n associated growth in health c a r e ex- penditures and in t h e number of sick-leave cases and disabled people.
I t is generally understood t h a t t h e causes of COPD are largely from within t h e society itself: life style (smoking), environmental ( a i r ) pollution, working condi- tions, and social and economic circumstances are believed t o b e responsible f o r
*Martin Rusnak, Research Institute for Medical Bionics, Jedlova 6, 883 08 Bratislava, Czechoslo- vakia
**Anatoli Yashin, IIASA, A-2361 Laxenburg, Austria
***P. Kristufek, Institute for Pneumophtisiology and Geriatrics, Podunajske Biskuplce, 82556 Bra- tislava, Czechoslovakia
t h e onsets of t h e s e c h r o n i c diseases. The growth in COPD p r e v a l e n c e is influenced by r e c e n t demographic t r e n d s , especially population aging.
The l a r g e p r o p o r t i o n of people with t h e s e sicknesses makes a complete regis- t r a t i o n of a l l tine cases a p r a c t i c a l impossibility. But COPD prevalence must b e es- timated in some way because of t h e necessity t o f o r e c a s t e and plan a p p r o p r i a t e health care r e s o u r c e s . We have developed a n a p p r o p r i a t e tool f o r t h e analysis of possible t r e n d s and d e s c r i b e COPD model in this p a p e r . The a u t h o r s hope t h a t i t will b e of some help in answering specific questions a b o u t COPD development. The model uses d a t a from t h e Slovak Socialist Republic and allows t h e u s e r t o test s e v e r a l s c e n a r i o s , as described in Chapter 7.
1. COPD EPIDEMIOLOGY IN SOME COUNTRIES
Much new information o n COPD and i t s e f f e c t on t h e health of t h e population h a s been revealed in numerous epidemiological studies. F o r example, i t w a s shown t h a t 17% of a l l British g e n e r a l p r a c t i t i o n e r s in t h e i r fifties have symptoms of COPD, as do 37.8% of o l d e r physicians ( P r i d e 1977); Hutli from Finland found COPD in 27%
of t h e population surveyed ( P r e s s and Rufener-Press 1974) and t h e prevalence of COPD in Sweden i s estimated t o b e l e s s t h a n 2% (Kirilog and I r n e l l 1974). Morbidity of chronic bronchitis in t h e US d i f f e r s according t o t h e areas surveyed and t h e chosen population groups: 23.5% in telephone companies' employees, 21.3% in t h e inhabitants of smaller industrial towns, 11% in r u r a l areas (Mueller et al. 1971).
Other American s u r v e y s have revealed t h a t 27% of t h e male and 13% of t h e female populations have symptoms a n d / o r spirometric abnormalities indicating COPD (Hig- gins and Keller 1970). Swiss d a t a f o r t h e male population in Geneva found t h e oc- c u r r e n c e of COPD t o b e between 2.7% in men 20-29 y e a r s old and up t o 7.7% in men o v e r 60 y e a r s old ( P r e s s and Rufener-Press 1974).
T h e r e have been s e v e r a l epidemiological studies of COPD prevalence in Czechoslovakia. In a group of 8298 men (52-67 y e a r s old) from P r a g u e , 32% were found t o have COPD. In r u r a l a r e a s , c a s e s were found in 24.8% of men 40-64 y e a r s old and in 7% of t h e women (Boudik et al. 1969b). From 1 9 7 1 t o 1975, a group of 20000 men 15 y e a r s and o l d e r (in t h e Czechoslovak area along t h e Danube r i v e r ) were checked f o r symptoms of COPD. Of t h i s group, 18.4% were diagnosed as hav- ing c h r o n i c bronchitis (Virsik et al. 1976).
The d a t a on COPD mortality does not adequately d e s c r i b e t h e importance of t h i s disease in t h e population. S e v e r a l f a c t s c a n explain t h i s situation:
Frequent coincidence of COPD with o t h e r , especially c a r d i o v a s c u l a r , diseases;
Many physicians tend t o r e f e r t o complications of COPD r a t h e r t h a n t h e main d i s o r d e r as a primary c a u s e of d e a t h (Fletcher et a l . 1964);
Sometimes t h e terminal bronchopneumonia o r o t h e r concomittant disease i s classified as a c a u s e of death instead of COPD (Herles 1964).
According t o Higgins (1973) 30-40 thousand d e a t h s p e r y e a r in t h e US are caused by c h r o n i c d i s o r d e r s of t h e pulmonary system. In Table 1 w e summarize t h e number of people who died from COPD in d i f f e r e n t c o u n t r i e s of t h e world in 1980
(WHO 1982).
Table 1. Number of d e a t h s from COPD in d i f f e r e n t c o u n t r i e s by s e x and a g e (WHO 1982).
Number of d e a t h s
Country Austria Bulgaria FRG Hungary Netherlands Poland
England and Wales Japan
Absolute P e r c e n t of all
Total Male Female Total Male Female
1710 1069 6 4 1 1.8 2.4 1.3
3647 2380 1267 3.7 4.4 2.8
22025 15079 6946 3.1 4.3 1.9
7043 443 2612 4.8 5.8 3.8
2750 2147 603 2.4 3.4 1.1
10096 7229 2867 2.8 3.8 1.8
20735 14802 5933 3.6 5.0 2.0
12712 8022 4690 1.7 0.2 1.4
Very important are t h e d a t a on o t h e r , i n d i r e c t indices of COPD morbidity, since, f o r example, 10% of all sick-leave in t h e US i s caused by COPD. 9 0 million US dollars are paid f o r sick leave t o invalids with c h r o n i c bronchitis (Higgins 1973) and t h e r e were 4.3 cases of COPD r e l a t e d sick-leave p e r 100 employees in F r a n c e in 1978 ( P e d r i z e t et a l . 1978). Recent estimates of COPD p r e v a l e n c e in t h e US give 1 0 million people and, collectively, c h r o n i c lung diseases account f o r more t h a n half a million hospital admissions annually. ' l h e limitation of activity o c c u r s l a t e r in life s o t h a t Medicare pays a l a r g e p e r c e n t a g e of t h e health care c o s t s (DHHS 1984). The i n c r e a s e in t h e number of sick-leave c a s e s , hospitalizations, and hospi- t a l d a y s f o r COPD in Czechoslovakia from t h e y e a r 1 9 7 1 i s illustrated in Figure 1.
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The continuous i n c r e a s e of all t h e indices is visible (CSSR zdravotnictvi 1983).
2. WHYA COPD MODEL?
Understanding t h e f a c t s and recognizing t h e importance of t h e effects of c h r o n i c , noninfectious diseases on t h e health s t a t u s of population led us t o design a COPD mathematical model. The aim of t h e model i s to facilitate t h e estimation of COPD p r e v a l e n c e and i t s development as t h e basis f o r c r e a t i n g a r a t i o n a l f o r e c a s t of health care development. I t could s e r v e as a test f o r v a r i o u s hypotheses about t h e development of t h e illness in t h e affected population. The s c o p e of t h e model i s b r o a d e r t h a n t h e health care system itself, since i t includes a s p e c t s of social c a r e , environment, and economics. This integrative a p p r o a c h introduces quantitative expressions f o r new ideas t h a t frequently a p p e a r in t h e l i t e r a t u r e on health care and clinical medicine. The model is based on a n understanding of t h e c a u s e s and r i s k f a c t o r s responsible f o r t h e onset and development of COPD.
3. CAUSES
AND
DEYELOPMENT OF COPDChronic o b s t r u c t i v e pulmonary disease is o n e of t h e typical illnesses in t h e developed world. I t s etiology i s usually d e s c r i b e d as multicausal. The e x a c t origin of t h i s t y p e of disease during t h e life span i s often undetectable which complicates t h e e x a c t disclosure of t h e causative f a c t o r . In t h e i r daily p r a c t i c e , medical doc- tors usually only face t h e full manifestations of clinical symptoms. The relation- ship of t h e s e manifestations t o t h e primary c a u s e s i s often impossible t o analyze in detail (Bajan 1968).
S e v e r a l epidemiological studies undertaken in various c o u n t r i e s have f u r t h - e r e d o u r understanding of many etiopathogenetic factors in COPD development.
From t h e clinical and p r a c t i c a l point of view, i t i s possible t o divide t h e s e into f o u r c a t e g o r i e s (Halak and Bajan 1976):
biological physical chemical allergical.
All of t h e s e f a c t o r s i r r i t a t e and infiltrate mucosis of t h e pulmonary system o r , through t h e antibody r e a c t i o n (allergy), p r e p a r e conditions f o r t h e illness t o develop (Ba jan 1983).
The above categorization of etiopathogenetic f a c t o r s i s especially suitable f o r didactic purposes, b u t in p r a c t i c e , one usually f a c e s t h e mixed e f f e c t s of t h e s e f a c t o r s . The e f f e c t of c i g a r e t t e smoke, f o r example. i s p a r t l y chemical, p a r t l y physical, and sometimes even allergical, which i s why we include t h e complex ef- f e c t s of t h e s e harmful a s p e c t s in t e r m s of a r i s k f a c t o r in t h e model.
3.1. Risk F a c t o r s f o r COPD D e v e l o p m e n t
Thanks t o t h e wide dissemination of warnings against smoking, c i g a r e t t e smok- ing is generally a recognized f a c t o r in t h e development of c h r o n i c airways diseases. Much less i s known of t h e o t h e r COPD r i s k f a c t o r s .
SMOKING: Smoking i s undoubtedly foremost in t h e etiopathology of COPD. The smoker c r e a t e s a n even h i g h e r contamination of a i r f o r himself by inhaling all t h e polluting substances from t h e smoke d i r e c t l y into his o r h e r airways. The number of harmful substances in c i g a r e t t e smoke i s given in Sylla (1978) and exceeds 1300 various kinds. Nicotine alone i s a s t r o n g enough poison, with l e t h a l doses of a b o u t 50 milligrams f o r a human being.
Functional abnormalities of t h e lungs are p r e s e n t in a l a r g e number of smok- ers (Fletcher et al. 1976; Dosman e t al. 1981; Tashkin et al. 1984). If they continue smoking, a significant number of them develop s e v e r e and clinically manifested ob- s t r u c t i o n s of t h e bronchial tree. Conclusions from s e v e r a l long-term prospective studies suggest t h a t cessation of smoking ( a t a n e a r l y s t a g e in c h r o n i c airflow development) c a n p r e v e n t progression t o a clinically significant disease by r e v e r s - ing t h e established, r e l a t e d a c c e l e r a t i o n in annual decline in t h e lung function t o o r toward a normal r a t e of decline (Fletcher and P e t o 1977; Bosse et al. 1981; Hjal- marson and Svardsudd 1981). Smoking significantly i n c r e a s e s t h e mortality of smokers. For heavy smokers (more than 2 5 c i g a r e t t e s p e r day), COPD r e l a t e d mor- tality is up t o 2 5 times h i g h e r t h a n f o r nonsmokers (Ferlinez 1974). This f a c t w a s demonstrated a l s o by Hammond (1966) in his study of 1 million males and females.
In Table 2 w e summarize t h e r e s u l t s of t h i s study and emphasize t h e difference in mortality between m a l e smokers and nonsmokers. In t h e female population t h i s difference w a s minimal.
Table 2. Mortality differences in smokers and nonsmokers by s e x and a g e (Ham- mond 1966).
Number of COPD d e a t h s
Non-smokers Smokers
Age Age
Sex 45-64 65-79 45-64 65-79
Male 1 0 1 0 194 1 7 5
Female 6
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Cigarette smoking acts alone and synergically with t h e o t h e r r i s k f a c t o r s of COPD. In t h e developed countries, i t i s t h e single most significant causal entity and i t s impol-tance is s e v e r a l times g r e a t e r than a i r pollution (WHO 1979).
AIR POLLUTION: People who live in u r b a n areas have a significantly h i g h e r incidence of COPD t h a n t h o s e from r u r a l a r e a s , as proved s e v e r a l times in epi- demiological surveys. The frequency of illnesses in airways i s much higher in t h e inhabitants of towns with e x t r e m e a i r pollution (Holland and Reid 1965). Air pollu- tion at t h e place of work plays a v e r y important r o l e , with symptoms of distur- bances of r e s p i r a t o r y functions being v e r y f r e q u e n t in miners and in workers in dusty environments. S e v e r a l studies have proved t h e dependence of COPD in- cidence on t h e length of employment in c e r t a i n high-risk professions. The r e s u l t s of investigation of COPD prevalence in t h e nonsmoking population of workers in c o a l / e l e c t r i c power plants, unambiguously s u p p o r t t h i s f a c t (Stejskal e t al. 1983).
The reversibility of t h e e f f e c t s of t h i s f a c t o r w a s proved in a study of mi- g r a n t s from towns with significantly polluted a i r in G r e a t Britain t o towns with less a i r pollution in t h e US (Reid and F l e t c h e r 1971).
A significant d e g r e e of a i r pollution c a n be achieved by smoking in closed rooms. Nonsmokers, being p r e s e n t in such a n environment, inhale cold c i g a r e t t e smoke with all t h e dangerous constituents, a phenomenon usually called passive smoking. Children with p a r e n t s who smoke a p p e a r t o have small, but measurable, differences in a test of lung function. These children a l s o have a n i n c r e a s e d f r e - quency of bronchitis, pneumonia, o r o t h e r r e s p i r a t o r y symptoms, when compared t o children from homes with nonsmoking p a r e n t s .
INFECTION: Despite t h e f a c t t h a t infection is not among t h e leading causes of COPD, i t s r o l e in t h e i n c r e a s e and development of t h e sickness i s generally recog- nized and proved (Tager and Speizer 1975). The r o l e and significance of b a c t e r i a l and v i r a l infection, from t h e etiopathogenetical point of view, i s demonstrated not only in t h e origin o f , but also in t h e maintenance of t h e c h r o n i c c h a r a c t e r of t h e COPD process. S e v e r a l a u t h o r s s t r e s s t h e significance of infections of t h e lower r e s p i r a t o r y t r a c t in childhood (Holland et al. 1969; Reid 1969). They t a k e into consideration t h e h i g h e r sensitivity in t h e s e children t o t h e development of COPD.
According t o t h e r e s u l t s of a study of 2228 schoolboys between t h e a g e s of 7 and 11 y e a r s (from South Wales and West England), up t o 10% of t h e boys and 6% of t h e g i r l s had infected airways. In t h e majority of t h e s e children, significant impair- ment of lung functions w a s found (Yarnell and Leger 1981).
ALLERGY: These f a c t o r s p r e s e n t independent and, until now, ambiguously solved problems. Despite plenty of new evidence, t h e r e i s no known mechanism t h a t c a n explain t h e complex of changes t h a t lead t o t h e final state of i r r e v e r s i b l e obstructive changes on t h e basis of atopy alone (Orie and von d e r Lende 1970;
Schmidt 1979).
AGE: In connection with t h e etiological f a c t o r s t h a t a f f e c t t h e development of COPD, i t i s n e c e s s a r y t o mention one more v e r y important factor-age. COPD f r e - quently o c c u r s in t h e o l d e r a g e category of t h e population. Conditions f o r t h e on- set of t h e manifestation of COPD c r e a t e , besides o t h e r f a c t o r s , physiological, s t r u c t u r a l , and pathophysiological changes in t h e lungs and in t h e bronchial t r e e during t h e l a t e r phases of life, as well as a g e n e r a l d e c r e a s e of r e s i s t a n c e .
GENETICS: In t h e e a r l y 1960s, s c h o l a r s announced a new syndrom--alpha 1 p r o t e a s e inhibitor deficiency being genetically t r a n s f e r r e d , later known under t h e t e r m a l p h a 1 antitrypsin deficiency (Laurel and Eriksson 1963). L a t e r on, t h e r e - lationship between t h i s d i s o r d e r and a significant i n c r e a s e in t h e size and reduc- tion of t h e number of alveoli, a diminution of t h e internal lung s u r f a c e , and a rear- rangement of t h e lung tissue was s t a t e d (Snider and Korthy 1978). I t is more t h a n probable t h a t t h e s e mechanisms play a n important r o l e in t h e c o u r s e of COPD (Snider 1984).
ALCOHOL: Burch and DePasquale (1967) hypothesized t h e existence of a n "al- coholic lung disease" and Rankin called attention t o t h e high prevalence of airways obstruction in alcoholics who a l s o smoke (Rankin e t al. 1969). Indeed, heavy al- cohol consumption i s associated with chronic c i g a r e t t e smoking in a l a r g e number of epidemiologic surveys. The association of heavy drinking with increased cough-
ing, excessive mucous hypersecretion, and frequent episodes of non-specific r e s p i r a t o r y illnesses h a s led numerous investigators t o speculate t h a t alcohol exa- c e r b a t e s t h e e f f e c t s of smoking and contributes t o t h e development of chronic bronchitis (Lebowitz 1981; Krumpe et al. 1984). Despite a l l of t h e r e s e a r c h being done in t h i s field, t h e question still remains open.
Etiopathogenetic f a c t o r s of COPD r e p r e s e n t a complicated s e t of agents of ex- ogenous o r endogenous c h a r a c t e r . They c o o p e r a t e in t h e i r originating changes in t h e bronchial tree and in c r e a t i n g t h e conditions f o r t h e individual forms and f e a t u r e s of COPD manifestation. T h e r e a r e still many open and unsolved questions in t h e etiopathogenesis of COPD, despite t h e evident p r o g r e s s of r e s e a r c h into t h e e f f e c t s and influence of d i f f e r e n t COPD r i s k f a c t o r s . N e w discoveries in t h i s field will not only have a t h e o r e t i c a l impact, but also a significant impact on prevention.
e a r l y diagnosis, and effective t h e r a p y .
4. COPD MODEL OBJECTIYES
Health care s t a t i s t i c s adequately d e s c r i b e t h e prevalence of tuberculosis, v e n e r e a l diseases, and communicative diseases in a majority of countries. This i s because when medical s t a t i s t i c s were developed, tuberculosis and infectious diseases were t h e most important health problems. This conjunction of medical s t a t i s t i c s and infectious diseases i s described in t h e curriculum vitae of Florence Nightingale, who helped t o pioneer t h e revolutionary notion t h a t social phenomena could b e objectively measured and subjected to mathematical analysis (Cohen 1984). Besides t h i s historical relationship, t h e r e i s a n o t h e r f e a t u r e of routine medical statisitics: t h e majority of them are episode based (case based), not based on t h e individual (Zacek 1984); modern health c a r e calls f o r knowledge of t h e l a t t e r t y p e of information. The prevalence image i s governed by chronic, noncom- municable diseases. However, no c u r r e n t routine s o u r c e of medical information treats t h e whole history of t h e development of a c h r o n i c disease from i t s onset un- til i t s end. Thus, health care managers frequently do not know t h e prevalence of a p a r t i c u l a r illness in t h e population. However, t h e y must have t h i s knowledge in o r d e r t o effectively fight against t h e illnesses.
P r e v a l e n c e studies are often used t o examine o c c u r e n c e s of c h r o n i c diseases, involving a limited proportion of t h e population who s u f f e r from a p a r t i c u l a r disease, disability, syndrome o r studied symptom within a s h o r t period of time. Of
' c o u r s e , such surveys a r e usually v e r y expensive, which i s why they a r e r e s t r i c t e d
in time and a r e a . The description of t h e allocation of a number of sick people is t h e usual r e s u l t a n d such information i s of g r e a t value f o r health care manage- ment. However, i t i s insufficient f o r t h e p u r p o s e of setting objective t a r g e t s and p r o c e d u r e s f o r t h e h e a l t h c a r e system and f o r s h o r t - and long-term planning, especially t h e latter.
In a r e c e n t p a p e r , w e drew attention t o t h e possibilities of using mathematical modeling to t r a n s f o r m s t a t i c information--which h a s been accumulated by means of d i f f e r e n t surveys--into a dynamic tool in t h e hands of health care managers (Koonce et a l . 1984). During t h e designing of t h e COPD model, w e h a v e k e p t in mind t h i s t a r g e t . The design i s based on understanding t h e c u r r e n t situation and defin- ing o u r aims. The g e n e r a l aim, remaining a f t e r a l l of o u r e f f o r t s , i s to d e c r e a s e t h e p r e v a l e n c e of COPD. To f u r t h e r this, t h e model c a n aid t h e t a s k of discovering t h e e f f e c t s of d i f f e r e n t r i s k f a c t o r s on COPD p r e v a l e n c e diminution. T h e r e i s probably no need f o r explaining t h a t i t has, besides t h e e t h i c a l consequences. such a diminution would have a s e r i o u s economic e f f e c t with r e s p e c t to t h e whole of so- ciety. The model a l s o follows t h i s a s p e c t of health care.
W e assume t h a t a f t e r some time t h e model will find i t s place within t h e system of continuous health-care development f o r e c a s t s . Even more, w e suggest t h a t t h i s model could b e used in p o s t g r a d u a t e training of health care managers at d i f f e r e n t levels. R e s e a r c h into COPD could p r o f i t from utilizing t h i s model as well.
5. COPD MODEL STRUCTURE
The COPD p r e v a l e n c e model consists of t w o m a j o r blocks of logic:
prognosis f o r population development
prognosis f o r t h e development of COPD r i s k f a c t o r s development.
The possibility of testing d i f f e r e n t s c e n a r i o s allows a holistic a p p r o a c h t o t h e model.
5.1. Population Development Prognosis
The f o r e c a s t i s based on a simplified view of population development. Data f o r t h e demographic prognosis are estimated from t h e number of newborns, t h e number of all d e a t h s , a n d t h e number of transitions between a g e groups. Such fac- t o r s as migration, male/female r a t i o , and s o on, were not considered in t h e f o r e -
-
11-
c a s t . The o v e r a l l prognosis is based on d a t a from Slovakia, 1983.
5.2.
COPD
Risk Factors PrognosisThis module r e p r e s e n t s t h e key point of t h e whole model. We have employed o u r knowledge of COPD etiopathogenesis in t h i s a r e a . The whole model construc- tion is according t o t h e following t h r e e population divisions: (1) healthy individu- als, (2) those in COPD r i s k , and (3) those suffering from COPD.
HeaLthy IndividuaLs: We define t h e members of t h i s group as those individu- a l s without COPD symptoms and those not under t h e influence of any of t h e r i s k fac- t o r s . We ignore t h e possibility of genetic t r a n s f e r of COPD, which means t h a t , from o u r point of view, all newborns a r e healthy, having t h e same probability of staying healthy o r entering any of t h e risk groups.
I n d i v i d u a L s w i t h COPD R i s k Factor: W e begin from t h e point of view of t h e model t a r g e t s in analyzing t h e problem of r i s k group selection. The only ones we selected were t h o s e with important etiopathogenesis and t h e real possibility f o r in- tervention by a health c a r e system o r society. That i s why w e c h o s e t h e following f a c t o r s :
smoking: one of t h e most important f a c t o r s , influencing t h e l a r g e s t p a r t of t h e population, but t h e e f f e c t of intervention by health c a r e o r society i s s t i l l dubious.
air poLLution: compared with smoking t h i s f a c t o r i s of secondary impor- tance. The r o l e of securing a diminution o r even elimination of t h i s i s of pri- m a r y importance.
f r e q u e n t r e s p i r a t o r y infections: t h e r o l e of t h i s f a c t o r in t h e development of COPD in adulthood i s still not clearly defined. In t h e s t r u g g l e against this f a c t o r , t h e last word h a s not y e t been said.
COPD s i c k i n d i v i d u a L s : Individuals who fulfil t h e WHO c r i t e r i a f o r c h r o n i c bronchitis, lung emphysema, o r bronchial asthma were placed in t h i s group (WHO 1980).
The o v e r a l l model s t r u c t u r e i s shown in Figure 2.
6. COPD MODEL REALKZATION
6.1. Model D e r i v a t i o n
The p a r t of t h e COPD model t h a t describes population dynamics i s based on t h e concept of people flow from one a g e category t o a n o t h e r in e a c h y e a r . A c e r t a i n number of people a r e b o r n and a c e r t a i n number die. Denoting as n l ( t ) t h e number of people in t h e group aged younger than 20 y e a r s , b ( t ) t h e number of newborns, and j+ t h e d e a t h r a t e f o r t h e f i r s t a g e c a t e g o r y in y e a r t , one c a n d e s c r i b e t h e population as follows:
n l ( t )
=
n l ( t -1)+
b ( t )-
0.05nl(t -1)-
h n l ( t -1).
(1)The constant 0.05 r e p r e s e n t s t h a t p a r t of t h e population which e n t e r s t h e next a g e group (20-year a g e g r o u p s in t h i s case). We do not h a v e newborns in t h e o l d e r ages, but instead we have a n inflow of people from t h e previous a g e groups. Be- cause we have 20-year a g e groups w e use t h e 0.05 constant again.
W e have only one transition from t h e l a s t group, s o w e c a n write t h e equation as follows:
The second p a r t of t h e COPD model d e s c r i b e s t h e dynamics of t h e population under different r i s k f a c t o r s . A s a l r e a d y mentioned, t h e people not subjected t o e x t r a r i s k of COPD development were considered as a special type. Denoting j f o r t h e a g e c a t e g o r i e s , one c a n d e s c r i b e this group as follows:
Assuming f o u r a g e c a t e g o r i e s , we have j
=
1 ,. . .
, 4. F o r those under 20 y e a r s of age, p denotes t h e number of newborns. F o r o t h e r s i t denotes t h e p a r t of t h e po- pulation t h a t e n t e r s t h e c a t e g o r y from t h e previous one:People from t h i s group may e n t e r one of t h e o t h e r risk groups, become ill from
COPD, or even die. The p r o c e s s of transition to o t h e r health h a z a r d s is r e p r e s e n t - ed by t h e sum of t h e transition coefficients p
The possibility of t h e onset of a COPD disease in healthy individuals i s depicted by t h e coefficient A!. The number of people dying in this group from causes o t h e r than COPD is:
when stands f o r mortality r a t e .
Applying similar notation, one can d e r i v e equations f o r estimating t h e number of c i g a r e t t e smokers:
1 1 2 2
n:(t)
= n;(t
-1)+
p nj( t ) +
p-
Aj nj( t
-1)-
0 . 0 5 n f ( t -1)- zjn:(t
-1)t h e number of people in a n air-polluted environment:
2 1
n;(t) =
n;(t -1)+
pn j ( t ) +
p-
A?n;(t -1)-
0 . 0 5 n f ( t -1)- -,nf(t
-1)and t h e number of children with frequent r e s p i r a t o r y infections:
3 1 4 4
n : ( t ) = n:(t-1) +
p nl( t ) -
A,n,(t -1) - 0 . 0 5 n : ( t - 1 )-&n:(t
-1).
(11) Since t h e aim of t h e model i s to estimate t h e number of people with COPD, t h e following equation w a s derived:-
15-
t o depict t h e COPD p r e v a l e n c e dynamics.
6.2. Implementation
The following items were used f o r t h e initialization of t h e f o r e c a s t :
a g e s t r u c t u r e of t h e population of t h e Slovak Socialistic Republic (SSR), 1983;
g e n e r a l d e a t h r a t e f o r population of SSR, 1983;
number of newborns in SSR, 1983;
number of COPD r e l a t e d d e a t h s in SSR. 1983;
r i s k of COPD in individuals in SSR, 1983, with and without r i s k f a c t o r s ; COPD r i s k - f a c t o r p r e v a l e n c e in t h e population of SSR, 1983;
coefficients of transition from t h e group without r i s k to t h a t with r i s k ; a v e r a g e length of s t a y in t h e hospital f o r a patient with COPD;
coefficient of transition from t h e group of COPD ill to disabled;
a v e r a g e number of d a y s in sanatoriums.
W e divide t h e population into f o u r g r o u p s according to age:
0-19 y e a r s ; 20-39 y e a r s ; 40-59 y e a r s ; 6 0 y e a r s and o v e r .
W e are a w a r e of t h e error possibly a r i s i n g from t h i s rough a g e s t r a t i f i c a t i o n , b u t r e s t r i c t i o n s d u e to t h e computer used did not allow us to p r o b e t h i s problem more deeply. The same situation o c c u r s in t h e s e x s t r u c t u r e . The following may s u p p o r t o u r decision not to consider s e x differences: in developed c o u n t r i e s smoking s t a r t e d as a predominantly male phenomenon and women s t a r t e d to smoke much l a t e r . While men were usually t h e f i r s t to s t o p smoking, smoking continued to i n c r e a s e among women (although i t h a s now s t a r t e d to level off, a p p a r e n t l y as a r e s u l t of smoking c o n t r o l activities) at a much lower rate t h a n t h a t r e a c h e d by men (WHO 1979). S o w e t r i e d to select d a t a describing t h e whole population r e g a r d l e s s of s e x .
In o u r model design, w e employed t h e assumption t h a t e a c h of t h e r i s k factors a f f e c t s t h e population independently. W e a b s t r a c t e d t h e i r synergistic e f f e c t s , having in mind t h e following ranking:
(1) smoking (2) a i r pollution
(3) f r e q u e n t r e s p i r a t o r y diseases in childhood.
So, if a n individual i s a smoker, i t i s possible to neglect t h e influence of o t h e r con- taminating f a c t o r s . Similar hypotheses were also a c c e p t e d f o r t h e o t h e r combina- tions of f a c t o r s , s i n c e t h e lack of d a t a on t h e effects of t h e combinations of r i s k s f o r c e s t h i s simplification.
W e implemented t h e COPD model on a n APPLE-IIe microcomputer in APPLESOFT BASIC. The program i s assembled from s e v e r a l modules, as shown in Figure 3. Data specifying t h e s t a r t i n g conditions of t h e model are i n c o r p o r a t e d i n t o t h e p r o g r a m by means of t h e command DATA.
6.3. Demographic Data
The demographic d a t a f o r t h e SSR population (age s t r u c t u r e , death rate, newborns) were e x t r a c t e d from t h e S t a t i s t i c a l Health C a r e Year Book f o r Czechoslovakia (CSSR zdravotnictvi 1983)*. Specific mortality f o r COPD w a s derived from a s t a t i s t i c s book (Pohyb obyvatelstva v SSR, 1983). The number of COPD d e a t h s i s not enumerated in t h i s book, which i s why w e considered t h e sum of d e a t h s from following diagnostic c a t e g o r i e s , according to t h e I n t e r n a t i o n a l Clas- s i f i c a t i o n o f f i s e a s e s (VIII-th revision):
ICD 491 c h r o n i c inflammation of bronchi-chronic bronchitis ICD 492 lung emphysema
ICD 493 bronchial asthma.
T h e r e are t h r e e t y p e s of mortalities considered in t h i s model: o v e r a l l mortali- t y , specific COPD mortality, and mortality without COPD. This distinction w a s em- ployed p a r t l y t o v e r i f y t h e d i f f e r e n t e f f e c t s on mortality and p a r t l y b e c a u s e of t h e possibility of extending t h e model to o t h e r diseases.
*These d a t a a r e included i n Table 3.
START
1
INPUT OF D A T A0 (
INPUT
NUMBER OF N FORECASTED YEARS
1
D E F I N I T I O N OF SCENARIO
POPULATION
RISK GROUPS A N D
I
PREVALENCE FORECASTI I
GRAPHIC?
O F RESULTS
RESULTS I N TABLES
Figure 3. The COPD model realization in computer program.
-
Table 3. Population, number of d e a t h s without COPD, and number of d e a t h s from COPD (Pohyb obyvateslstva v SSR 1983).
Initial demographic d a t a f o r Slovakia, 1983
Age g r o u p Population in SSR Deaths without COPD COPD d e a t h s
0-19 1736000 3342 1
20-39 1619000 1912 7
40-59 1070000 6735 1 2 3
60- 731000 33269 1760
6.4. Number o f COPD Cases
T h e r e are two main channels of information about g e n e r a l morbidity data:
routine s t a t i s t i c s special investigations
Most c o u n t r i e s d o not supply routine d a t a on COPD p r e v a l e n c e (Shigan 1977). How- e v e r , t h e d a t a d o d e s c r i b e hospitalizations, sick-leave cases a n d days, disease specific mortality, and o t h e r i n d i r e c t measures of prevalence. The most a p p r o p r i - ate s o u r c e of p r e v a l e n c e d a t a are s p e c i a l investigations. W e based t h e estimation (of t h e initial COPD p r e v a l e n c e in t h e SSR) on t h e r e s u l t s of a study of 20000 inha- bitants, 15 y e a r s and o l d e r , in t h e Danube area (Virsik et al. 1976) along with a n investigation of a b o u t 60000 people (male and female) in t h e West of Slovakia (Kru- t y et al. 1975). For a more p r e c i s e estimation of prevalence, w e plan a n extension of t h e model with a module of p r e v a l e n c e estimation based on some i n d i r e c t p r e - valence indices. The values of t h e initial COPD p r e v a l e n c e are summarized up in Table 4.
6.5. Risk o f D e v e l o p i n g COPD
W e consider t h e estimation of coefficients-for expressing t h e r i s k of COPD development in a n individual s o r t e d by r i s k factors--to b e of c r u c i a l value f o r t h e s u c c e s s of t h e model. The way t h a t w e p e r c e i v e t h e r i s k considers t h e pathogenic power of t h e etiology f a c t o r , which means t h e magnitude of r i s k f o r a n individual
Table 4. Initial COPD p r e v a l e n c e in Slovakia, 1983.
Age Number of cases
s u b j e c t to one of t h e f a c t o r s t h a t i n c r e a s e s t h e likelihood of developing t h e con- s i d e r e d disease. According to Zacek (1984), t h e measure of r i s k i s according t o t h e magnitude and duration of t h e association. Mathematical s t a t i s t i c s o f f e r a number of d i f f e r e n t techniques f o r establishing t h i s (Armitage 1971). Case-control and c o h o r t studies are used to measure t h e i n c r e a s e d r i s k of i n c u r r i n g a particu- lar disease if a c e r t a i n f a c t o r i s p r e s e n t . In c o h o r t studies, s u c h estimations c a n b e done d i r e c t l y by observing t h e e x p e r i e n c e of g r o u p s of s u b j e c t s with and without t h e f a c t o r . In a case-control study t h e d a t a d o not p r e s e n t a n immediate answer t o t h i s t y p e of question. The association between t h e f a c t o r and t h e d i s e a s e could b e measured by t h e r a t i o of t h e r i s k s of t h e d i s e a s e being positive f o r t h o s e with and t h o s e without t h e f a c t o r .
W e p r o c e s s e d coefficients of r e l a t i v e COPD r i s k according to d a t a from COPD epidemiological studies c a r r i e d o u t in t h e SSR during r e c e n t y e a r s . Because w e could not find a s u r v e y of t h e consequences of all t h r e e r i s k f a c t o r s used, w e com- bined d a t a from s e v e r a l s o u r c e s . Numerous s u r v e y s were conducted to compare t h e incidence and r i s k of COPD in t h e inhabitants of r u r a l and u r b a n areas (Olejni- c e k et al. 1974; Kubik et al. 1978; Coufal et al. 1973). W e solved t h e question of COPD incidence in youths with t h e help of a study o r i e n t e d selectively on younger a g e c a t e g o r i e s (Vyslouzil et al. 1975). For t h e r i s k of COPD development in indivi- duals with f r e q u e n t r e s p i r a t o r y infections during childhood w e used t h e r e s u l t s of t h e study on t h e population of South Wales and t h e West of England (Yarnell and Leger 1981), because w e do not know of any such s u r v e y in Slovakia. Table 5 con- tains values of coefficients used.
Table 5. Risk of COPD onset f o r people under different r i s k s , by age.
Age
Risk group 0-19 20-39 40-59 60-
Without r i s k 0.02 0.1 0.2 0.25
Smokers 0.05 0.3 0.6 0.75
Air pollution 0.1 0.2 0.25 0.3
Respiratory infections 0.39 0 0 0
6.6. Risk Factors Prevalence
The estimation of risk-factor incidences in t h e population could, at f i r s t glance, b e r e g a r d e d as a n e a s i e r task compared t o previous ones, but w e have t o state rational limitations t o b e successful. T h e r e a r e a l a r g e number of s u r v e y s t h a t consider t h e distribution of smokers in t h e population. Different c l u s t e r s of smokers a r e used according t o , e.g., what i s smoked, f o r how long, how deeply t h e smoke is inhaled, e t c . W e made use of t h e following stratification of people ac- cording t o t h e i r smoking habits:
smokers nonsmokers
W e r e s t r i c t e d o u r attention t o c i g a r e t t e smoking alone. W e received some valuable d a t a on smoking from t h e Special Study of Tobacconism in Slovakia (Ka- t r i a k 1983). They investigated t h e smoking habits of 1700 inhabitants of t h e SSR 14 y e a r s and o l d e r , chosen at random according to s e x , age, social s t a t u s , and residential area. The study r e p r e s e n t s a complex view on smoking epidemiology in t h e SSR.
More problems were faced in estimating t h e number of people affected by pol- luted a i r . For Slovaks living in areas with good quality a i r and f o r those living in towns with proved a i r pollution, no a p p r o p r i a t e d a t a were found. W e understand t h a t this division is t o o general, but until b e t t e r d a t a i s available w e c a n use noth- ing else. The d a t a on a i r pollution were estimated according t o Kiihnl (1982).
The frequency of r e s p i r a t o r y diseases in children i s about 3-4 illnesses p e r y e a r , but i s usually less f r e q u e n t f o r children in r u r a l areas. W e estimated t h e number of children with f r e q u e n t r e s p i r a t o r y infections with t h e help of a pediatrician's e x p e r t estimation. Our opinion, based on e x p e r i e n c e with t h i s d a t a
estimation, i s t h a t no more p r e c i s e d a t a on t h a t problem will b e available in t h e n e a r f u t u r e . The p r o p o r t i o n s of people s u b j e c t t o d i f f e r e n t r i s k s are summarized in Table 6.
Table 6. P r o p o r t i o n s of people s u b j e c t t o d i f f e r e n t r i s k f a c t o r s by a g e .
- A g e - - -
Risk g r o u p 0-19 20-39 40-59 60-
Smokers 0.144 0.277 0.245 0.07
Air pollution 0.273 0.161 0.130 0.045
R e s p i r a t o r y infections 0.264 0 0 0
6.7. T r a n s i t i o n C o e f f i c i e n t s B e t w e e n G r o u p s
These coefficients d e s c r i b e how a n individual s u b j e c t t o none of t h e mentioned h e a l t h r i s k s c a n e n t e r o n e of t h e r i s k groups. Derivation of t h e s e c o e f f i c i e n t s i s b a s e d on t h e assumption t h a t a newborn child i s u n d e r n o r i s k , which e x c l u d e s t h e possibility of h e r e d i t a r y d e f e c t s . Numbers f o r t r a n s i t i o n s to t h e g r o u p of s m o k e r s were d e r i v e d from t h e a l r e a d y mentioned study of c i g a r e t t e smoking epidemics in Slovakia (Katriak 1983). The estimation of coefficients f o r air pollution w a s d o n e using migration d a t a f o r Slovakia (Kiihnl 1982). Because of t h e l a c k of s t a t i s t i c a l d a t a on c h i l d r e n ' s r e s p i r a t o r y infections, e x p e r t opinions were used. The e x p e r t s (physicians) were familiar with t h e epidemiological situation among t h e c h i l d r e n in Slovakia. Table 7 comprises t h e d e s c r i b e d coefficients f o r Slovakia.
Table 7. Coefficients of t r a n s i t i o n s between t h e g r o u p of people with no mentioned h e a l t h h a z a r d compared t o t h o s e with h a z a r d .
Age
Risk g r o u p 0-19 20-39 40-59 60-
To s m o k e r s 50 30 30 30
To air-polluted areas 0.025 0.06 0.06 0.165 To r e s p i r a t o r y infections 0.08 0 0 0
7. RESULTS AND DISCUSSION
The COPD model allows t h e u s e r t o f o r e c a s t t h e p r e v a l e n c e development t o t h e y e a r 2003 (20 y e a r s f o r e c a s t ) . Figure 4 d e p i c t s t h e b a s i c development of p r e - valence, when no interventions are assumed. Notice t h e steady i n c r e a s e in quanti- ty of sick people, especially in a g e categories, which. should s t r i k e t h e attention of health care managers and policymakers.
S e v e r a l s c e n a r i o s were used t o test different a p p r o a c h e s and t h e i r impacts on t h e population. The transformation of a n e x p e r t ' s ideas into s c e n a r i o s r e p r e s e n t s a quantification of t h e hypothesis, and i t i s possible t o e x p r e s s such a quantification in s e v e r a l d i f f e r e n t ways. The model uses p e r c e n t a g e s as a measure of change between t h e original state and t h e hypothetical situation. The change could b e introduced in any y e a r of t h e f o r e c a s t e d period.
Tested hypotheses w e r e chosen in o r d e r t o highlight t h e answers t o t h e s e questions:
how would a change in t h e amount of people a f f e c t e d by d i f f e r e n t r i s k s influ- e n c e COPD p r e v a l e n c e in t h e f u t u r e ?
how would t h e p r e v a l e n c e react t o a change in more effective COPD t h e r a p y and prevention?
Figures 5 and 6 d e p i c t situations in which d i f f e r e n t changes in t h e smoking si- tuation are assumed. The hypotheses of reducing t h e number of smokers and of in- c r e a s i n g t h e smoker population were t e s t e d . Reducing t h e amount of people af- f e c t e d by c i g a r e t t e smoke h a s long been a t a s k of many, not necessarily health care, a u t h o r i t i e s all o v e r t h e world, with s e v e r a l programs of WHO and o t h e r insti- tutions trying t o treat t h i s problem. US smoking habits are shown in Table 8.
Column (1) of Table 8 shows t h a t t h e t o t a l US c i g a r e t t e consumption h a s in- c r e a s e d f a i r l y steadily o v e r t h e p a s t t w o decades, but t h e growth in t o t a l consump- tion h a s not k e p t p a c e with t h e growth in t h e smoking population. This i s r e f l e c t e d in column (3) in which t h e a g g r e g a t e d a t a are converted into c i g a r e t t e s p e r adult (individuals o v e r 1 7 y e a r s of age). A s columns (3) and (4) show, by t h i s measure c i g a r e t t e consumption h a s fallen steadily, if gradually, since 1 9 7 3 (Warner 1983).
Figure 5 shows t h e p r e v a l e n c e change a f t e r t h e effective antismoking cam- paign w a s introduced (dimunition of smokers t o 80% in people younger t h a n 20 y e a r s and t o 70% between 20-39 y e a r s of a g e in t h e y e a r 1985).
Table 8. Total and adult p e r c a p i t a c i g a r e t t e consumption by y e a r (Warren 1983).
T o t a l consumption P e r c e n t a g e i n c r e a s e P e r c e n t a g e i n c r e a s e ( b i l l i o n s of ( d e c r e a s e ) f r o m Consumption ( d e c r e a s e ) from c i g a r e t t e s ) preceding y e a r p e r adult preceding y e a r
Year (1) (2) (3) (4)
The awaited e f f e c t of dimunition of COPD c a s e s w a s not as significant as one might have hoped. Nevertheless, a d e c r e a s e of 1000 COPD sick people in t h e younger a g e g r o u p s will h a v e a more significant e f f e c t on t h e i r health when t h e y become o l d e r . P r a c t i c a l l y no change w a s achieved in t h e o l d e r a g e c a t e g o r i e s , which r e f l e c t s t h e time delay r e q u i r e d f o r -an individual from o n e a g e g r o u p to r e a c h t h e o l d e r a g e c a t e g o r y . A s w e have 20-year a g e groups, only a half of t h e population will r e a c h t h e o l d e r a g e g r o u p s during t h e f o r e c a s t e d p e r i o d (10 y e a r s ) .
The s c e n a r i o with increasing numbers of smokers in two younger-age c a t e g o r i e s w a s t e s t e d ( t h e number of people younger t h a n 20 y e a r s who start smoking i s i n c r e a s e d by 140% and t h a t of people between 20-39 y e a r s of a g e by 130% of t h e 1985 figures). The r e s u l t s were just t h e opposite to t h o s e derived from t h e f i r s t s c e n a r i o , as shown in Figure 6.
COP0 CASE S [THOUS
NDSJ
YEARS OLD
I Ff,FNII
- - - - .
-- -
NO SCENARIO---XENARIG
COPD CASES
M J W
1200- a
59 YEARS1
9001
a
1
80.
NO S C E W I [ )I SCE WIO
4
4
J 1 1 1 1 1 1 1 1 1 A
1063 6c 85 & 87
86
6990
91a
R J ~ [ I E * ~ COPD CASESM J W
Ul 59 YEARS
F i g u r e 5.
C O P D U S E S
/~MOUSANDS/
1 2-
4
I
900.
a
600-
LEGEND
4 a
--- -
NO SCENARIO SCENARIO300-
a
COPD CASES EwNDSI
12001
40-59
YEARS OLD.I
.I
m
600- LECEH)
-
NO SCENARKIm
--
SCENARIOF i g u r e 6.
The most a f f e c t e d population would b e in t h e younger-age c a t e g o r i e s . The hy- pothesis used r e f l e c t s a situation t h a t i s common in n e a r l y a l l t h e developed coun- t r i e s . The number of heavy smokers among men in twenties and t h e i r t h i r t i e s in- c r e a s e d , but t h e number among o l d e r men d e c r e a s e d . The number of female heavy smokers, o n t h e o t h e r hand, h a s continued to i n c r e a s e s until women were in t h e i r fifties (Stoto 1985).
Another two s c e n a r i o s t e s t e d t h e situations in which substantial changes in COPD prevention and t r e a t m e n t effectiveness o c c u r . Screening f o r initial lung function impairments and complex t r e a t m e n t of a c u t e u p p e r r e s p i r a t o r y infections t o g e t h e r with decreasing a i r pollution, are t h e main possibilities f o r preventing COPD illness. Figure 7 r e f l e c t s t h e situation with i n c r e a s e d effectiveness of preventive programs. The usual t a r g e t of such programs i s t h e adult p a r t of t h e population--up t o 60 y e a r s of age. The hypothesis employed suggests t h e r i s e in prevention effectiveness will b e 140% in t h e a g e groups 20-39 and 40-59 y e a r s . The r e s p o n s e of t h e model w a s immediate. The change w a s introduced in 1984 and a sig- nificant d e c r e a s e in COPD p r e v a l e n c e a p p e a r e d during t h e same y e a r in t h e second and t h i r d a g e c a t e g o r i e s and a f t e r f o u r y e a r s in t h e o l d e r a g e categories.
Assuming t h a t t h e h e a l t h a u t h o r i t i e s will not pay a p p r o p r i a t e attention t o t h e preventive activities, t h e hypothesis of a decline to 60% of t h e c u r r e n t s t a t u s in t h e same a g e g r o u p s as t h e previous s c e n a r i o w a s tested. The change w a s intro- duced in 1984 and t h e r e s u l t s of t h e f o r e c a s t are shown in Figure 8.
CONCLUSIONS
More hypotheses t h a n mentioned h e r e were checked, most s t r i k i n g r e s u l t s be- ing given as examples of t h e model's r u n s . The d e s c r i b e d model i s o n e of t h e f i r s t s t e p s in o u r e f f o r t s t o model sociodemographic impacts of c h r o n i c diseases on po- pulations. The r e s u l t s showed u s what w e should u s e in f u t u r e population models.
Based on t h e experiments with t h e model, t h e following conclusions c a n b e drawn:
t h e model provides t h e experimentor with meaningful f o r e c a s t s and enables him o r h e r t o test d i f f e r e n t t y p e s of scenarios;
t h e COPD model i s sensitive enough to simulate assumed changes;
COP0
CASESLEGE ND
-
NO SCENARIO---
SCENARIOF i g u r e 7 .
COPD CASES
L f ~ u ~ m
w
1200-
-
a
900-
.I
COO-
OLD
Figure 8 ,
t h e d a t a aggregation by f o u r a g e groups seems t o us t o b e t o o c o a r s e , disaggregation into more a g e groups and by s e x would probably bring b e t t e r insights into t h e system dynamics;
t h e disaggregation would certainly r e q u i r e more computer memory t h a n 64 K b y t e s and t h e use of some compilor seems t o b e n e c e s s a r y , because of t h e in- c r e a s e d time f o r computation;
t h e i n t e r a c t i v e , user-friendly mode of t h e model's o p e r a t i o n allows i t s utiliza- tion by those unskilled with computers.
The incomplete information on COPD p r e v a l e n c e and on t h e transitions between d i f f e r e n t population groups does not allow to use t h e traditional model- tuning p r o c e d u r e s . The r e s u l t s of modeling, however, were discussed with e x p e r t s in COPD, whose opinion was t h a t t h e model i s r e a l i s t i c and can help in understand- ir\g t h e mechanisms of COPD development. The new d a t a on v a r i o u s a s p e c t s of COPD will allow u s to develop a more detailed version of t h e model.
Based on t h e s e f a c t s , t h e new version of t h i s model i s u n d e r p r e p a r a t i o n . The a u t h o r s hope t h a t i t will b e of substantial help t o o t h e r s c h o l a r s in t h i s field.
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