Before 16 weeks of gestation, intrauterine events can impact the number of airways. One example of a congenital lung disease is congenital diaphragmatic hernia, which occurs between 6 to 8 weeks of gestation. This condition arises when the pleuroperitoneal canal fails to close, resulting in the mixing of the chest and abdominal cavities. As a consequence, the lung hemithorax contains abdominal contents, leading to abnormal lung growth with a decrease in the number of airways and alveoli. Prior to birth, the alveolar epithelium solely consists of type II epithelial cells, and it is only after birth that these cells differentiate into type I epithelial cells.

Lung growth is closely related to the growth in body length and stature, progressing proportionally. The fastest development rate occurs during the neonatal and preadolescent periods, with girls maturing earlier than boys. While lung growth slows after adolescence, both the body and lungs continue to increase in size until adulthood. Throughout the growth process, lung function improves. However, once optimal size is reached in early adulthood (around 20 to 25 years of age), lung function starts to decline with age. This decline is estimated to be less than 1% per year and tends to occur earlier and progress faster in individuals who smoke or are exposed to toxic environmental factors. Aging primarily affects ventilatory capacity and responses, particularly during exercise, resulting in abnormal ventilation despite normal perfusion. Additionally, gas diffusion decreases with age, likely due to a reduction in alveolar surface area. The age-related decrease in lung function and altered structure align with biochemical findings of increased elastin levels in the lung, which could explain some of the functional abnormalities.

Type I cells lack free radical scavengers and are susceptible to injury and death caused by toxic oxygen compounds and free radicals. In various inflammatory lung diseases, type I cells die, leading to denudation of the alveolar epithelium, increased vascular permeability, and subsequent fluid accumulation, ultimately impairing gas exchange. Type II cells possess superoxide dismutase and are therefore more resistant to toxic oxygen radicals. They have the ability to survive, proliferate, and differentiate into type I cells to restore normal alveolar architecture. This response depends on the presence of an intact basement membrane, which supports the proliferation of type II cells. It is an example of "phylogeny recapitulating ontogeny." If the basement membrane cannot be repopulated, the body resorts to collagen deposition and scar formation for repair, which is not conducive to gas exchange.

The lungs exhibit both anatomical and physiological unity, with each bronchopulmonary segment being structurally identical and functioning in the same manner as the others.

The upper airways, consisting of the nose, sinuses, and pharynx, condition inspired air by adjusting its temperature, humidity, and atmospheric pressure. They also control the flow of air into the lungs and food/fluids into the esophagus through the epiglottis.

The lower airways, including the trachea, bronchi, and bronchioles, are considered conducting airways responsible for transporting air to the gas-exchanging respiratory units, which comprise respiratory bronchioles, alveolar ducts, and alveoli.
Thus intrauterine events that occur before 16 weeks of gestation will affect the number of airways. A condition known as congenital diaphragmatic hernia is an example of a congenital lung disease. It occurs at 6 to 8 weeks of gestation and is due to failure of the pleuroperitoneal canal to close and thereby separate the chest and abdominal cavities; the presence of the abdominal contents in the lung hemithorax results in abnormal lung growth with a decrease in the number of airways and alveoli. Before the birth of an affected infant, the alveolar epithelium is composed solely of type II epithelial cells, and it is not until birth that these cells differentiate into type I epithelial cells.
Growth of the lungs is similar and relatively proportional to growth in body length and stature. The rate of development is fastest in the neonatal and preadolescent periods (≈11 years of age), and girls’ lungs mature earlier than boys’. Although the growth rate of the lung slows after adolescence, the body and lung increase in size steadily until adulthood. Improvement in lung function occurs at all stages of growth development; however, once optimal size has been attained in early adulthood (20 to 25 years of age), lung function starts to decline with age. The decrease in lung function with age, estimated at less than 1% per year, appears to begin earlier and proceed faster in individuals who smoke or are exposed to toxic environmental factors. The major physiological insufficiencies caused by aging involve ventilatory capacity and responses, especially during exercise, and they result in abnormal ventilation with normal perfusion. In addition, gas diffusion decreases with age, probably as a result of a decrease in alveolar surface area. Age-related decreases in lung function and altered structure parallel biochemical observations of increased levels of elastin within the lung, which could explain some of the functional abnormalities.
TypeIcellslackfreeradicalscavengers(i.e.,superoxidedismutase)andaresusceptibletoinjuryanddeathinducedbytoxicO2compoundsandfreeradical(i.e.,H2O2,OH− ,andO2−).Invariousinflammatorylungdiseases,typeIcellsdie,andthealveolarepitheliumtherebybecomesdenuded,withincreasedvascularpermeabilityandensuingfluidaccumulation(impairedgasexchange).TypeIIcellshavesuperoxidedismutaseandarethusmoreresistanttothetoxicoxygenradicals.TheycansurvivetoproliferateanddifferentiateintotypeIcellstorestorethenormalalveolararchitecture.ThistypeofresponseisdependentonanintactbasementmembranetosupporttheproliferationoftypeIIcellsandisanexampleof“phylogenyrecapitulatingontogeny.”Ifthebasementmembranecannotberepopulated,thenthebody’srecourseforrepairiscollagendepositionandscarformation,whichisnotconducivetogas 1.
The lungs demonstrate anatomical and physiological unity; that is, each unit (bronchopulmonary segment) is structurally identical and functions just like every other unit.
2.
The upper airways (nose, sinuses, pharynx) condition inspired air for temperature, humidity, and atmospheric pressure, and they control, via the epiglottis, the flow of air into the lungs and food/fluids into the esophagus.
3.
Components of the lower airways (trachea, bronchi, bronchioles) are considered conducting airways in which air is transported to the gas-exchanging respiratory units composed of respiratory bronchioles, alveolar ducts, and alveoli.
4.