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Poor Lung Function at Birth a Risk for Adult COPD


TUCSON, Ariz. -- For many adults with poor airway function or COPD, the genesis of the problem may have been in the womb, researchers reported.

TUCSON, Ariz., Aug. 31 -- For many adults with poor airway function or COPD, the genesis of the problem may have been in the womb, researchers reported.

Poor airway function shortly after birth should be recognized as a risk factor for later airflow obstruction and COPD and may result from poor fetal lung development, Fernando D. Martinez, M.D., of the University of Arizona here, and colleagues, reported in the Sept.1 issue of The Lancet.

Although the factors that affect pulmonary development in utero are not well understood, maternal smoking during pregnancy has been consistently associated with poor lung function in both infants and children, the researchers said.

Their findings emerged from a non-selective longitudinal study of 169 infants enrolled at birth in the Tucson Children's Respiratory Study from 1980 through 1984.

The researchers measured maximal expiratory flows at functional residual capacity (VmaxFRC) by the chest compression technique at a mean of 2.3 months.

They also obtained measurements of lung function for 123 participants at least once at 11, 16, and 22 years.

The measurements were forced expiratory volume in 1 second

(FEV1), forced vital capacity (FVC), forced expiratory flow between 25% and 75% of FVC, and forced expiratory flow (FEF25-75), both before and after treatment with a bronchodilator (180 ?g of albuterol).

After adjustment for height, weight, age, and sex, the researchers found that at ages 11, 16, and 22, infant airway function accounted for 9% to 14% of the variability in subsequent adjusted spirometric lung function measures.

Participants who had an infant VmaxFRC in the lowest quartile also had lower values for the FEV1/FVC ratio (?5.2%, P<0.0001), FEF25-75 (?663 mL/s, P<0.0001), and FEV1 (?233 mL, P=0.001) up to age 22, than those in the upper three quartiles combined.

Moreover, the researchers said, individuals who had low airway function as infants had much greater responses to bronchodilators than did others.

The magnitude and significance of this effect did not change after additional adjustment for wheeze, smoking, atopy, or parental asthma.

Although a strength of the study was the large proportion of participants available after birth and in young adulthood, the researchers noted that they were unable to accurately determine the relative contributions to lung function in early adult life of congenital deficits in airway function and of acquired factors such as lower respiratory infections, ongoing symptoms, and environmental exposures.

However, the investigators said, these findings support the hypothesis that factors that control airway development in utero determine the degree of airway function an individual will attain by early adult life.

This hypothesis, they said, meets the observation that branching of the bronchial tree is complete by 16 weeks of gestation, and that the number of terminal bronchiolar duct endings does not increase after birth.

In addition, they said, these results suggest that in-utero alterations in airway development predispose an individual both to lower respiratory illnesses and to deficiencies in lung function during adult life.

"We postulate that even if lung function were to diminish during adult life at rates similar to those recorded in non-smokers, they would reach the threshold that defines COPD at an earlier age than their peers," the researchers wrote.

The factors that affect pulmonary development in utero are not well understood, they said. Lung morphogenesis is a highly regulated process that could be impaired in utero by both genetic and environmental factors, including maternal smoking during pregnancy.

These results suggest that a better understanding of the mechanisms that control normal lung growth in fetal life would contribute to development of strategies for the prevention of chronic obstructive pulmonary disease in adult life, Dr. Martinez and his colleagues concluded.

In an accompanying comment, Michael Silverman, M.D., of the University of Leicester in England, and Claudia E. Kuehni, M.D., of the University of Bern, Switzerland, wrote that the study raises several questions about the nature of the impairment, beyond airway function, in neonatal and adult lung function.

For example, reduced pulmonary elastic recoil might contribute to reduced flow, they said.

Also, they asked, what are the fetal causes of impaired lung growth beyond maternal smoking, such as environmental and genetic causes? They pointed out that only 9-14% of the variability in spirometric lung function at age 22 as explained by neonatal forced expiratory flows, leaving much room for other childhood exposures in the COPD pathway.

This study, they wrote, leaves room for other childhood exposures in the COPD pathway, such as lower-respiratory illness in young children, preschool viral wheeze, and asthma.

"As COPD is set globally to become the third most important cause of death, now is the time to add research into its earliest origins to the agenda," they said.

Drs. Silverman and Kuehni declared no conflicts of interest.

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