Removing the obstructions: a life course approach to preventing COPD

By J.J. Keith

SYD 5136

7 December 2009

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Abstract

This paper consists of a formal review of the literature on the etiology of COPD,

followed by a discussion of COPD within the context of life course studies. Building on the

literature review and discussion, a possible prevention strategy to take place over the life

course is suggested.

Introduction

Imagine a disease which is non-communicable, but nearly one in twenty Americans has

it. The WHO estimates that in 1990, Chronic Obstructive Pulmonary Disease was the twelfth

most burdensome disease in the world, but by 2020, it is expected to become the fifth (Murray

& Lopez 1997). COPD is just that and is likely to be much more endemic than the health care

community is aware, since it is also highly underreported and under-diagnosed (Pena et al.

2000). COPD is characterized as a chronic, irreversible obstruction of the airway system.

Symptoms include inflammation and hardening of the various components of the pulmonary

system, fluid buildup, mucus secretion, frequent headaches, sleep apnea, hypoxia and dyspnea.

It is a debilitating disease for which there is no cure. The Center for Disease Control and

Prevention has recorded over 12 millions current cases of COPD in the United States, and they

also estimate that another four million people have it but do not know it (Murray & Lopez

1997). COPD is the fourth leading cause of deaths in the US, behind heart disease, cancer and

cerebrovascular disease. What is shocking is that while the death rates of these other diseases

are either decreasing or holding steady, the rate of deaths from COPD is rising steadily (Pauwels

et al. 2001). However, there are many ways to prevent it, assuming preventive care is

implemented before it is too late. In order to understand how it works and why so many people

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suffer from it, it is necessary to understand the comorbidities upon which diagnosis is

dependent.

The purpose of this paper is to review the etiology of COPD and its comorbidities, profile

the unique gradient in the social distribution of the disease, and describe how it relates to the

life course and how a life course approach to treating the disease will help to reduce

inequalities in its susceptibility. This paper will then conclude by imagining an intervention

strategy suggested by a life course perspective.

Etiology

Like most hubristic diseases, the disease prevalence of COPD is not socially distributed

evenly across age, class, race, ethnicity or gender. For instance, the very nature of the disease’s

development and progression over the life course puts the elderly at an increased risk. The

etiology portion of this paper is broken up into five sections. The first section describes how the

disease is diagnosed, as the real threat posed by COPD is not the coughing or the infections, but

rather based on deteriorated lung function. The second section will discuss global and regional

endimicity. The third section will review the comorbidities associated with COPD. The Fourth

section will be a brief overview of the environmental agitators, with a substantial emphasis on

smoking, smoking being the fifth section. Smoking has its own section because it has been

shown that smoking plays a critical role in development of the disease and also is one of the

primary sources for the gradient in the social distribution of COPD.

Diagnosis

The Forced Expiratory Volume Curve (FVC) is a graph of air exhaled against time (see

Graph 1). The reasoning behind this is physiological; the amount of air one can exhale can never

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be more than one can inhale. Since the exchange rate of oxygen and carbon dioxide is relatively

stable, a decreased lung function means that less oxygen is brought in with each breath and

more carbon dioxide is left in the body (Alonso

et al 1992). This is why COPD patients

experience dyspnea (shortness of breath) and

hypoxia (decreased cellular oxygenation), which

causes the headaches and inhibits metabolism,

ultimately asphyxiating cells. This process is

concentrated in the lung tissue, exacerbating

the issue geometrically. During sleep, this lack

of oxygenation is viewed by the body as a decreased need to breathe, causing sleep apnea.

While deaths by asphyxiation during sleep are much more common in older ages, COPD

patients at all ages are at an increased risk for asphyxiation during sleep, depending on the

severity of the disease. It is within this context that COPD patients suffer until death and also

drag down with them their loved ones and society at large.

Endimicity

COPD is not evenly distributed globally. As Table 1 demonstrates, the World Health

Organization estimates that COPD is more prevalent in developed nations than developing

nations. This could be caused by a number of reasons, two of which seem to be most likely. One

is the possibility of underreporting in developing nations. It is common knowledge that

healthcare in developing nations is of much lower quality than in developed nations. Therefore,

patient confidence in medicine will likely vary; if a doctor does not feel that anesthesia is

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necessary for childbearing or tubal ligation, then what would be the point in asking to treat a

chest infection or persistent cough? Further, most of the debilitation of COPD – dyspnea and

fatigue – is associated with age anyway. Why not assume that the person is just getting old

instead of suffering from some abstract disease that only rich nations get? The other possible

cause for the global gradient might be that developed nations, while typically more health-

conscious, do have a much greater potential for generating the fumes which exacerbate COPD,

like fossil fuel emissions and tobacco smoke. Combining these two scenarios, underreporting

and overexposure, offer a more intuitive explanation for why developed nations might suffer

more than developing nations.

Building on the unequal global endimicity of COPD, there has been a similar relationship

observed with respect to level of community development. US Department of Vital Statistics

records show that, within developed nations, COPD is more endemic in rural regions of

developed countries than urban. This may seem paradoxical, but smoking is much more

prevalent among the poor than other socioeconomic statuses. Typically, poverty in developed

nations tends to be concentrated in rural areas where jobs and education are less prevalent

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than in urban areas. The problem of smoking among the poor will be given special attention in

this paper.

Comorbidity

In order to be diagnosed with COPD in the US, ICD-9 parameters specify that a patient

must first be diagnosed with chronic bronchitis. That having been said, a brief explanation of

how chronic bronchitis insults the pulmonary system must be touched on here. According to

IDC-9 standards, chronic bronchitis is characterized by a frequent inflammation of the airways

into the lungs (bronchial tubes), typically caused by viral infection. Symptoms include persistent

wet cough, mucus build-up in the bronchial tubes and occasional fever. When the mucus builds

up, the airway is restricted, mimicking the airway constriction of COPD. The persistent cough

stresses the bronchial tubes, often inflaming them, again constricting the airway like COPD.

By and large, the signs and symptoms of COPD include those of asthma, with the

exception of asthma attacks. Also, an analysis of Medicaid claims of COPD conducted by Du and

colleagues (2008) presents strong evidence in support of asthma, both adolescent and adult-

onset, as a common comorbidity of COPD. In fact, Pena and colleagues (Pena et al. 2000)

presented a method of detecting underdiagnosis of COPD by measuring spirometry,

bronchodilation and FVC of asthma patients. Their results revealed that, in addition to a

startling underdiagnosis of COPD in general, there was a much higher underdiagnosis rate of

COPD among asthma patients than non-asthma patients.

Another prerequisite comorbidity is emphysema. This disease is characterized as an

over-inflation of the alveoli – like a rubber band dry-rotting – and a subsequent hardening of

the alveoli and other lung tissue. This process often is the result of prolonged exposure to

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hazardous fumes, most commonly carbon monoxide and carbon dioxide, but also build-up of

inorganic particles in the lungs. Concentration of these gases in toxic levels is often found in

two places: certain occupations and smoking. Emphysema does not happen at once; while the

lungs may harden due to sudden extreme overexposure, such as being in a fire, most

emphysema patients are diagnosed because of a lifelong exposure to a number of hazardous

fumes (McClure and Anderson 1957).

Smoking

Each of the diseases discussed thus far have a number of physical stimuli which

exacerbate both themselves and COPD as well. Among these are pollen (Gilmour et al. 2006),

fungal spores (Delfino et al. 1997), cockroaches (Alark et al. 1999), air pollution (Brauer et al.

2001), climate (Hales et al. 1998; Egleston et al. 1999),and thunderstorms (Celenze et al. 1996),

among many others. However, the most potent and common of the culprits is tobacco

smoking, which has been shown to be

a precipitator of chronic bronchitis

(Flodin et al. 1995), emphysema

(Wagena 2004), asthma (Mitchell &

Stewart 2001) and COPD (Tzounou et

al. 1992). It has been estimated that

smoking is responsible for 1 in 5 deaths

in the developed world (Peto et al.

1992). Given the recent array of data on smoking and its inherent dangers (Liguori & Hughes

1996), why do people continue to smoke? This question will be dealt with later in this paper.

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Social distribution of COPD

As earlier stated, COPD is not distributed equally among social class, gender, race,

ethnicity or age. Table 2 represents the findings of the IBERPOB Multicentre Epidemiological

Study of COPD prevalence in Spain. Similarly, a study on Medicaid claims for COPD and asthma

conducted by Du and colleagues (2008) found generally the same trends for gender, smoking

and age, but also reported that white people tend to be diagnosed with COPD more than

African-Americans and other non-whites. Bear in mind that the study by Du and colleagues

focused on Medicaid patients, so at the bottom socioeconomic class, COPD is more prevalent

among whites than non-whites. In effect, COPD it seems targets older white males in the rural

parts of developed nations who either smoke or used to smoke.

COPD over the life course

As has been demonstrated thus far, COPD does not happen all at once. There are many

other prerequisite comorbidities which in themselves take years to gestate. Coincidently, these

diseases tend to correspond with a critical period in the life course, aligning to the critical

period model by Rice and Barone (2000). From infancy and adolescence through youth on into

participation in the labor force, the trajectory leading to COPD often plays a deciding factor in

the transition to retirement or, in many cases, disability.

Infancy – Asthma

Clark and colleagues (1999) have done substantial work in laying out what factors

determine whether someone becomes asthmatic. Effectively, the primary cause outside of the

womb is overburdening of the pulmonary system during its development. When the lungs of a

child are developing, the tissue is very sensitive to the air it takes in, and while the immune

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system is strong, the relative sensitivity to inorganic particles and gases – namely fossil fuel

smog, pollen and tobacco smoke – causes the airways in the lungs to tighten up regularly. As

the lungs continue to develop, they are conditioned to a predisposition of being tightened and

hypersensitive. The old saying “what doesn’t kill you makes you stronger” does not apply here.

In fact, these insults actually accumulate to predispose one to hypoxia, dyspnea and general

shortness of breath.

Adolescence- chronic bronchitis

Lundback and colleagues (1993) have conducted a thorough analysis of the relationship

between asthma and chronic bronchitis, and how both are tied to COPD. They have done this

using data from the Study of Obstructive Lung Diseases in Northern Sweden. Their results, like

many others, demonstrate that while the two diseases insult lung function in different ways –

through developmental conditioning in asthma and increased susceptibility to viral infections in

chronic bronchitis – those who test positive for chronic bronchitis are more likely to have

asthma than those who register an otherwise healthy bronchial system. The researchers

noticed that this trend was also geographically polarized, with both a higher prevalence rate

and a higher underdiagnosis rate in the north. They then concluded that it was environmental

factors (Northern Sweden is partly above the Arctic Circle) which contributed to the enhanced

prevalence of asthma and bronchitis. In effect, Lundback and colleagues attribute the

comorbidity of asthma and bronchitis to a common set of environmental precipitators. Their

sentiment is shared in much of the literature on the relationship between the two.

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Labor force participation – emphysema

Once a person has developed both asthma and chronic bronchitis, they are well on their

way to other pulmonary diseases like emphysema and COPD, but these diseases are not

necessarily unavoidable. The ability to prevent emphysema and COPD will be later discussed.

This section of the paper is devoted to an otherwise separate path: the one leading to

emphysema. According to McClure & Anderson (1957), “patients with moderately severe

pulmonary emphysema, who are getting along relatively well, may develop acute severe

pulmonary insufficiency with the onset of an acute lower respiratory infection. In other words,

their pulmonary reserve is so poor that a simple chest cold may tip the scale” (p. 597).

Emphysema itself has been characterized as an overinflation and a subsequent hardening of the

alveoli, and while this may not in itself cause one to become sick, it does put one at a greater

risk.

Emphysema, like the other pulmonary diseases, has been tied to smoking. However, the

tie between smoking and emphysema is much stronger than the other diseases, as

demonstrated by Anderson and colleagues (1964). Their explanation is that smoking is a

cumulative insult to the pulmonary system, its greatest disservice being done to the alveoli.

While each drag deposits a negligible sum of carbon and other hazardous particles, which the

lungs can clear out over time, a habitual smoker will smoke several cigarettes per day,

depositing particles at a pace which the lungs cannot continually process. As the particles

accumulate, they break down the alveolar walls, causing emphysema. Though it is associated by

many as the main cause for emphysema, smoking is not the only culprit. Other common causes

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of emphysema include airborne mineral particles (Churg et al. 1997), diesel fumes (Hart et al.

2006), and ambient air pollution (Brauer et al. 2006).

Unlike asthma and chronic bronchitis, emphysema has a social distribution similar to

COPD; it is most prevalent among poor white males in rural parts of developed nations (Marley

1966). At this point it should be noted that morbidity and mortality from emphysema is greater

than COPD, chronic bronchitis and asthma. In 1999, the National Vital Statistics Report

extrapolated that an average of 48 people died each day from emphysema complications.

Transition to retirement – COPD

The transition from emphysema and chronic bronchitis to full-blown COPD is a rather

common one, but it is also the best place to intervene, as it is possible to prevent COPD even

with emphysema and chronic bronchitis. Just having the two does not by default give one

COPD. It has been demonstrated by Toevs and colleagues (1984) that a patient with both

prerequisite diseases can be treated and with rigorous therapy including ephedra and quitting

smoking, it is possible to prevent the onset of COPD and even reverse the symptoms of

emphysema and chronic bronchitis once a person is diagnosed with both. Once a true decrease

in lung-function is observed over time, the diagnosis is imminent. The COPD patient

transitioning to retirement may or may not have a say in when they leave the workforce or if

they even make it to retirement age. Recalling that the average COPD patient is 53 years of age,

the debilitating effects COPD has on its patients can lead to diagnosed functional disability.

Persson and colleagues (2005) have found from their research that the average COPD patient is

diagnosed as physically disabled earlier than their peers who do not have COPD. They have also

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learned that the overall level of disability for COPD patients is higher at all age groups when

compared to non-COPD patients.

Life course approach to preventing COPD

In order to level the gradient in the social distribution of COPD, one must understand

the disease trajectory which leads to COPD in these cases. A critical point to intervene would be

immediately following diagnosis of emphysema. It is thus important to understand the

mentality of an emphysema patient. According to Nett and Petty (1970), Emphysema patients

tend to be career manual laborers, live at or below the poverty line, smoke regularly and work

in environments hazardous to the pulmonary system, such as processing plants, mines and

around fossil fuel fumes. For those who do not smoke, the prime cause of COPD is occupational

particles and fumes. The logical course of action to prevent COPD in these patients would be to

have them transfer jobs or at least begin to wear respirators while on the job.

Smoking cessation

In the other hand, the vast majority of COPD patients smoke, and since it has been

demonstrated that smoking is more hazardous to the lungs than most other precipitators, an

aggressive non-smoking campaign is in order for them. Despite an already aggressive global

campaign to reduce smoking rates, it may still come as a surprise to individuals just how

hazardous smoking is to a person’s health. Thus, a targeting of typical COPD candidates for

education and awareness, especially in more aged populations in rural areas where smoking

rates are more prevalent and thus more socially acceptable, would be a step in the right

direction.

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 However, Chaloupka (1991) has resigned himself to the fact that some people simply

will not give up tobacco. In these cases, people tend to defend their habit by blaming it on peer

pressure and salience of family attitudes (Chuang et al. 2005), claiming that it reduces stress

and allows them to make it through the day (Rothenbacher et al. 1996), as well as many other

things. While this may or may not be true, DiClimente (1993) has reviewed the literature on

addictive behavior and, in his discussion, has expounded on the concept of counter-

conditioning, in which one stress-coping mechanism is substituted for another. So instead of

smoking when one feels anxious or stressed, an alternative – say doctor-prescribed medication

or simply talking out one’s stress – would replace the smoker’s desire to smoke. Or, if the

person insists on tobacco, there are alternatives, such as chewing, dipping or even nicotine

patches. Recently an electric, smokeless cigarette has been introduced on the market. It works

by heating up a nicotine packet and then vaporizing it. This allows the smoker to absorb

nicotine through the lungs just like in smoking, only without the additives normally present in

tobacco smoke, like tar, cyanide, carbon monoxide, and various others. However, no

quantitative study has been conducted on this electric cigarette to see if it actually negates the

side-effects of smoking.

Life course prevention strategy

As earlier stated, a life course approach to reducing inequalities in the social distribution of

COPD would really mean preventing COPD in the largest cohort – white, working-poor males.

To intervene in the disease trajectory over the life course would mean also intervening in the

disease trajectory for asthma, chronic bronchitis and emphysema as well. Returning to the

critical period model, the ideal time to intervene in each of these diseases would be to head

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them off before they are diagnosed. This would mean identifying individuals on the path to

asthma – preterm white male adolescents born into a poor home life – and implementing an

asthma prevention strategy, which might include offering free in-home air purifiers. If that does

not work and the child is diagnosed with asthma, then focusing on preventing chronic

bronchitis during youth would be the next step in the life course prevention strategy. The most

effective strategy here would be to treat any respiratory infections as soon as symptoms

appear by visiting the doctor for antibiotics as early as possible. If that does not work and the

youth is diagnosed with chronic bronchitis, then the next step in the life course strategy would

be to intervene in the emphysema trajectory. This would include the aforementioned

aggressive anti-smoking campaign, plus use of a respirator when working around chemicals or

hazardous fumes. If that fails and the patient is diagnosed with COPD, then the final strategy

would be to litigate for disability and remove the patient from exposure to irritants as

thoroughly as possible.

Measurement

How would a life course intervention strategy like this look? Step one would be to pick

out the white, working-poor class males and approach their parents about participation. Once a

substantial sample has been recruited, mothers would be encouraged to breastfeed their sons

for at least four months, as a relationship has been observed between length of breastfeeding

and prevalence of asthma (Oddy et al. 1999). At the same time, air-purifiers would be handed

out. This would limit exposure to hazardous airborne irritants in the home at least. If the child

makes it to youth does not develop asthma, then he is dropped from the program, and counted

as “not surviving” the COPD trajectory. This method of applying age-appropriate intervention

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throughout the critical period will continue until all participants are either dropped from the

program or die from COPD.

Figure 1 represents a

measurement by means of a

survival curve (Motulsky

1995) accompanied by a chart

of treatment and hypothetical

number of survivors.

Conclusion

Since the symptoms of chronic bronchitis and emphysema separately overlap those of

COPD but develop at different stages of the life course, then treating them as one developing

trajectory is necessary. Since the prevalence of the three diseases also tends to target the same

social entity – poor white males in rural parts of the developed world – then successfully

preventing COPD in this social sector would mean reducing the overall prevalence rate. Finally,

the intervention strategy put forth in this paper requires a life course time frame because the

trajectory of COPD begins at birth, if not in the womb, and tends to develop over the entire life

course, plaguing the patient and deteriorating health until death.

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