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Host factors
• Age
• Susceptibility genes (e.g. alpha-1 antitrypsin deficiency)
• Poor lung growth and development (especially in neonatal life)
• Poor nutrition
• Low socio-economic status
Exposure
• Tobacco smoke
• Indoor air pollution from heating and cooking with coal and wood in poorly ventilated dwellings
• Outdoor air pollution
• Occupational dusts and chemicals
• Respiratory infections
• socio-economic status
The role of tobacco smoke as a causative agent for COPD has been proven beyond all doubt. It appears that starting smoking at a young age, the "total pack years" (the number of cigarettes smoked per year multiplied by the number of years of smoking) and the person's current smoking status all contribute to the final state of respiratory impairment due to COPD.
In spite of this, only an estimated 20% of smokers develop the disease. However, this figure does not take into consideration the combined effect of several other risk factors that commonly occur in individuals in underprivileged communities, with a subsequent greater likelihood of developing the disease.
Evidence has been found that secondary cigarette smoke can cause COPD in non-smoking bystanders. This has serious health and legal implications, as smokers could jeopardise the health of the non-smoking population.
In a number of occupations, including mining and industry, dust and exposure to welding gases and fumes have been associated with the development of COPD. Enforcement of protective measures in the workplace, including wearing masks and monitoring levels of dust and toxic fumes, have minimised and in some cases abolished the danger of industrial exposure.
Low socio-economic status is a risk factor for the development of COPD due to the high prevalence of other risk factors, including secondary cigarette smoke exposure, particularly in childhood, and tuberculosis, which tends to occur in deprived communities.
There is some evidence that tuberculosis (TB), particularly recurrent episodes of the disease, leads to the development of COPD in patients in developing countries.
Additional risk factors in disadvantaged communities include the indoor burning of biomass fuels and a tendency to recurrent chest infections, which in their own right cause further damage to the bronchial walls and contribute to the onset of COPD. In these communities, children of parents who smoke are at a proven disadvantage, as recurrent chest infections and impaired lung growth predispose these unfortunate individuals to early development of COPD.
The fact that many industrial workers and miners smoke and contract tuberculosis serves as one example of how combinations of risk factors contribute through a final common pathway of airway inflammation to create an accumulative burden for causing COPD.
It should be evident that as long as these risk factors prevail in communities, the disease prevalence will continue its upward spiral and continue to be a major burden on national and personal health budgets.
There is also growing evidence that HIV infection, either alone or together with other opportunistic infections and tuberculosis, may be an independent risk factor for the development of COPD. Whether this is due to repeated respiratory infections, the effect of the virus on the lung tissue itself, or simply the result of decreased immunity is unknown, and is currently under investigation. This interaction obviously has enormous public health implications for a country like South Africa, with its high rate of both HIV and TB.
(Written by Prof J.R. Joubert, MSc, MBChB (Stell), FCP (SA), MMed (Int. Med), MD (Stell.))
(Reviewed by Dr Greg Calligaro, physician at the Lung Unit, Groote Schuur Hospital and University of Cape Town, August 2010)
• Age
• Susceptibility genes (e.g. alpha-1 antitrypsin deficiency)
• Poor lung growth and development (especially in neonatal life)
• Poor nutrition
• Low socio-economic status
Exposure
• Tobacco smoke
• Indoor air pollution from heating and cooking with coal and wood in poorly ventilated dwellings
• Outdoor air pollution
• Occupational dusts and chemicals
• Respiratory infections
• socio-economic status
The role of tobacco smoke as a causative agent for COPD has been proven beyond all doubt. It appears that starting smoking at a young age, the "total pack years" (the number of cigarettes smoked per year multiplied by the number of years of smoking) and the person's current smoking status all contribute to the final state of respiratory impairment due to COPD.
In spite of this, only an estimated 20% of smokers develop the disease. However, this figure does not take into consideration the combined effect of several other risk factors that commonly occur in individuals in underprivileged communities, with a subsequent greater likelihood of developing the disease.
Evidence has been found that secondary cigarette smoke can cause COPD in non-smoking bystanders. This has serious health and legal implications, as smokers could jeopardise the health of the non-smoking population.
In a number of occupations, including mining and industry, dust and exposure to welding gases and fumes have been associated with the development of COPD. Enforcement of protective measures in the workplace, including wearing masks and monitoring levels of dust and toxic fumes, have minimised and in some cases abolished the danger of industrial exposure.
Low socio-economic status is a risk factor for the development of COPD due to the high prevalence of other risk factors, including secondary cigarette smoke exposure, particularly in childhood, and tuberculosis, which tends to occur in deprived communities.
There is some evidence that tuberculosis (TB), particularly recurrent episodes of the disease, leads to the development of COPD in patients in developing countries.
Additional risk factors in disadvantaged communities include the indoor burning of biomass fuels and a tendency to recurrent chest infections, which in their own right cause further damage to the bronchial walls and contribute to the onset of COPD. In these communities, children of parents who smoke are at a proven disadvantage, as recurrent chest infections and impaired lung growth predispose these unfortunate individuals to early development of COPD.
The fact that many industrial workers and miners smoke and contract tuberculosis serves as one example of how combinations of risk factors contribute through a final common pathway of airway inflammation to create an accumulative burden for causing COPD.
It should be evident that as long as these risk factors prevail in communities, the disease prevalence will continue its upward spiral and continue to be a major burden on national and personal health budgets.
There is also growing evidence that HIV infection, either alone or together with other opportunistic infections and tuberculosis, may be an independent risk factor for the development of COPD. Whether this is due to repeated respiratory infections, the effect of the virus on the lung tissue itself, or simply the result of decreased immunity is unknown, and is currently under investigation. This interaction obviously has enormous public health implications for a country like South Africa, with its high rate of both HIV and TB.
(Written by Prof J.R. Joubert, MSc, MBChB (Stell), FCP (SA), MMed (Int. Med), MD (Stell.))
(Reviewed by Dr Greg Calligaro, physician at the Lung Unit, Groote Schuur Hospital and University of Cape Town, August 2010)
