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Childhood Lung Disease and Urban Environmental Pollutants

Reference: Charles G. Plopper, and Michelle B. Fanucchi, June 2000. Do Urban Environmental Pollutants Exacerbate Childhood Lung Disease? Environmental Health Perspectives. A252-A253. Vol: 108, (6).

The editorial cited above was prompted by the recent finding that repeated exposures of young rhesus monkeys to ozone and house dust mite aerosol results in permanent remodeling of the distal conducting airways in the lung.1 The authors conclude that this could be the pathophysiological basis for findings of decreased small airway function reported in a group of college students who grew up in the Southern California Air Basin. They urge more governmental resources be devoted to the study of lung disease in children after presenting 6 factors possibly related to the increase in childhood lung disease in the United States.

The recent increase in lung disease in children in the United States appears to be related to the effect of 3 biological factors and 3 environmental factors. Discussion of the biological factors leads to the conclusion that the early postnatal lung is more susceptible to permanent lung damage from environmental pollutants than the adult lung. These factors are as follows:

1- The human lung continues to develop for 6 to 8 years after birth. The same events essential in prenatal development occur during this postnatal period. Thus known prenatal sensitivities are present for up to 8 years in the lung after birth.

2- The genetic diversity of the population is now being defined. Some genotypes are associated with increased susceptibility to asthma.

3- There is increased sensitivity of the neonatal lung of experimental animals to environmental pollutants. In addition the normal repair processes of the adult lung, including cell proliferation, are diminished in neonates. This occurs in spite of decreased levels of xenobiotic-activating enzymes in neonatal lungs relative to adult lungs.

The environmental factors thought to interact with the above biological factors are as follows:

1- There seems to be an increase in both complexity, distribution, and levels of such pollutants as irritant gases and respirable particulate matter including tobacco smoke and diesel exhaust of various aerodynamic diameters. However, there are few studies concerning the effects of such combinations of pollutants on neonatal lungs.

2- There is an increase in identified allergens such as products derived from house dust mites and cockroaches.

3- Endotoxins are prevalent both indoors and out and are known to alter critical interactions of the airway epithelium and interstitium necessary for proper development. There are currently no data on the levels of environmental endotoxins in past years.

Drs. Plopper and Fanucchi conclude that the above three environmental factors in concert with the three lung biology factors act synergistically in the etiology of childhood pulmonary disease, especially childhood asthma.  To ensure the future health of the US population, more governmental resources must be devoted to study the effects of low levels of combinations of environmental pollutants on the lungs of neonatal animals.

1.  Fanucchi, MV, Wong, VJ, Hinds, D, Tarkington, BK, Van Winkle LS, Evans, MJ, Plopper, CG.  Repeated episodes of exposure to ozone alters postnatal development of distal conducting airways in infant rhesus monkeys.  Am J Respir Crit Care Med 161:A615(2000).

By: Susan G. Shami, ScD