Rate of decline in lung function

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Typically, FEVj reaches a peak at around age 20-25 and then gradually declines with age by approximately 20-30mL/year. Little, however, is known about the lung function of existing individuals with COPD in the decades be fore the disease becomes apparent. It seems logical that patients with COPD may have reached their low FEV1 by one of the following three routes.

1 An accelerated decline in lung function. In their classic paper that followed 800 London office staff with serial measures of FEV1 over 8years, Fletcher et al. [38] demonstrated that there is a range of FEV1 decline per year from almost nil to over 100mL per year. They suggested that those with a rapid decline were susceptible smokers. The average decline was 18mL greater in a smoker than in a non-smoker, i.e. 54 mL vs. 36mL/year. Some non-smokers showed a rapid decline in function, indicating that there are factors other than smoking to be considered, but there were many more rapid decliners amongst the smokers and it is only those with very rapid declines (i.e. of 70-100 mL per year) who can lose the 3L or more of lung function that places them in the FEV11-litre category that is seen with hospital admissions of patients in their sixties.

The rate of decline is not linear over a lifetime. In the young, FEV1 may rise between 20 and 25, followed by a relative plateau, before falling at an initially slow but accelerating rate over the years. Thus, the average rate of fall in FEV1 described in a cohort may be describing an average between small gains in the youngest and large falls in older subjects. This makes it difficult to compare different studies. There are few longitudinal studies to compare with that of Fletcher et al.

The US Lung Health Study [39] observed 4000 patients with mild COPD over 5 years with and without an anticholinergic bronchodilator. While the drug had no effect on rate of loss of FEV1, the authors did note as a secondary end point that the rate of loss of FEV1 was significantly less in those who quit smoking compared to those who continued. They also observed that those with bronchial hyperreactivity had an increased rate of loss compared to those without. Thus, both exogenous and endogenous factors may affect the rate of decline. As a generalization, the average fall in FEV1 in susceptible smokers seems to be in the order of 60 mL per year (i.e. twice that of non-smokers) [40].

The cross-sectional studies of smokers and non-smokers have also found a greater loss of lung function amongst smokers. Many have applied linear regression analysis to the data in an attempt to determine the additional aetio-logical factors responsible. This must be viewed with caution—firstly because the rate of loss is not uniform, and secondly because the starting point for different cohorts is unknown. An analysis of decline in a Dutch community study [41] reported that there was a significant effect depending on when a person was born. Men born a generation later tended to be 2 cm taller and to have 360 mL more FEV1 —presumably a reflection of better socio-economic condi tions and better conditions in childhood. Few studies include year of birth as a variable, and thus the cross-sectional analysis performed on the raw FEV1 data would wrongly attribute this loss to another cause.

2 Premature decline in lung function. All parts of the human body deteriorate with increasing age, and the lung is no exception. Humans also age at different biological speeds, and perhaps one of the most promising areas for future research is the genetic basis of COPD. Accelerated loss of lung function in smokers with a1-antiprotease deficiency was first recognized by Laurell and Eriksson in 1963 [42]. This autosomal-recessive condition (ZZ phenotype) is found in 0.03% of the UK population. The lung is rendered susceptible to damage from neutrophil elastase, typically causing rapidly progressive emphysema in homozygotes who smoke. The heterozygotic state MZ is found in 3.9-14.2% of COPD patients, compared with 1.2-5.3% of controls (odds ratio 1.2-5.0). Other genetic predispositions are very likely to exist. Silverman et al. have reported a three-fold increased risk of developing COPD among first-degree relatives that is unrelated to a1-antiprotease status [43]. A family history of chronic bronchitis was shown by Carrozzi et al. to be associated with impaired FEVj in smokers [44]. Other postulated genetic mechanisms include polymorphisms in the tumour necrosis factor-a gene, the microsomal epoxide hydrolase gene and the glutathione S-transferase P1 gene.

3 Impaired lung growth and therefore a decrease in the peak lung function attained. Insults to the developing lung during childhood, including premature birth and infection, may have a role. In a study of 700 people with a mean age of 70, Shaheen et al. [45] reported that pneumonia before the age of two was associated with a mean reduction in FEV1 of 0.65L in men, compared with controls. In women, the reduction was smaller and non-significant. In South Wales, children who had admissions for infections as children had an increased risk of dying 60 years later of COPD. Whether it is the infections themselves that are to blame or problems in utero is not known, but there is one study that suggests that poor nutrition in utero is a factor. Barker et al. noted that low birthweight was predictive of an increased risk of dying of COPD 60 years later [46].

It is of great concern therefore that women who smoke are known to have smaller babies with an increased incidence of prematurity—this may be placing their children at risk of COPD long before the children have a chance to make decisions for themselves.

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