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Over the last two decades, the potential influence of inadequate nutrition on lung structure and function has been extensively explored. Knowledge o f nutrition-related pulmonary changes is based mainly on animal studies.

2.7,2,1 Animal studies

Fetal lung metabolism increases dramatically near term when glucose oxidation serves as the most important source o f energy fuel (Hamosh et al. 1981). When rat fetuses were exposed to prolonged periods o f nutritional deprivation during critical periods o f growth, Simmons et al. demonstrated that glucose transport was spared in the brain but diminished in the fetal rat lungs, thus possibly affecting lung growth (Simmons et al. 1992).

Evidence has also been reported that pre-natal under-nutrition is associated with delayed cytodifferentiation o f epithelial cells, decrease in lung phospholipid content and negatively interferes with pulmonary surfactant production (Faridy, 1975; Lin and Lechner, 1991; Guamer et al. 1992). The effects o f pre-natal underfeeding on the formation o f terminal air spaces varies with both animal species and timing o f malnutrition and this has led to much contradictory evidence in the literature (Curie

and Adamson, 1978; Lin and Lechner, 1991). Morphometric analyses do, however, reveal that prenatally starved animals have a significantly reduced volume and surface area o f parenchymal components as adults, even though catch up growth occurs once normal feeding is resumed (Kalenga et al. 1999). In a study to investigate the effects o f intrauterine deprivation on aspects o f structural development of the trachea and lungs o f fetal sheep, Rees et al. found abnormal development o f the trachea, particularly affecting the mucosal and submucosal layers. There was frequently a lack o f a ciliated border on epithelial cells in the mucosal layer and a reduction in the extent o f the folds usually characteristic o f this layer in near term fetal sheep (Rees et al. 1991). Furthermore, in a recent study, near term sheep fetuses in whom lUGR was induced by umbilico-placental embolization were shown to have a thicker air-blood barrier (Harding et al. 2000) and lower total DNA content than controls (Cock et al. 2001). However, pulmonary DNA concentration (per g o f lung weight) in the lUGR group was elevated compared to controls (Cock et al. 2001). The authors proposed that as pulmonary DNA concentration decreases during normal gestation, the higher pulmonary DNA concentration in the lUGR group suggests that the lungs in these fetuses were structurally immature.

Dietary lipids are also critical for fetal lung development as fatty acids play an essential role in the structural and functional dynamics o f fetal lung cells towards maturation (Nelson et al. 1980). During early lung development, lipids play an important role in protecting against oxidant-induced lung injury. Pregnant rats fed with diets enriched with polyunsaturated fatty acids have been shown to have better tolerance for hyperoxia as newborns (Sosenko et al. 1988).

There is increasing evidence that Vitamin A (retinol) and its metabolite, retinoic acid, are major factors involved in differentiation and in the maturation o f the lungs (Chytil, 1992). In his review, Chytil reported that Vitamin A is involved with pulmonary gene expression and that lack o f this dietary micronutrient causes keratinizing squamous metaplasia of the bronchopulmonary tree that can be reversed by refeeding the animal with retinol. In addition. Vitamin A is an essential factor in the regulation o f type II pneumocyte proliferation (Zachman, 1995). Conversely, prenatal hypervitaminosis A has been shown to cause thickening o f septal walls with

atelectasis in fetal lung parenchyma (Kalenga et al. 1999). Similarly, trace elements such as selenium are involved in fetal and neonatal lung development and deficiency of this element may result in lung growth retardation with septal attenuation (Kim et al. 1991).

2.7.2.2 H um an observations

Currently, there is little information on the influence o f specific nutrients or micronutrients on human fetal lungs or infant airway development, relative to animal data presented earlier. One form of fetal malnutrition is intrauterine growth restriction, resulting in infants who are small for gestational age.

Post-mortem studies o f the newborn infants who are underweight have shown that their lungs are lighter than expected for body weight although alveolar development appeared appropriate for gestational age (Gruenwald, 1963). In a study undertaken of people bom around the time of the Dutch famine in 1944-5 to determine the effects o f maternal malnutrition, the prevalence o f obstructive airways disease was increased in people exposed to famine in early and mid gestation (Lopuhaa et al. 2000). It has also been suggested that fetal malnutrition may impede growth of conducting airways. Barker et al reported that FEVi was significantly reduced in adults aged 59-70 years whose birth weight was < 2500 g, even after adjusting for age, height, smoking habits and social class (Barker et al. 1991). Impaired airway function in relation to low birth weight was also reported in adult Indians (Stein et al. 1997). These data suggest that maternal and fetal nutrition may influence fetal lung growth and development. However, in humans it is not known how much o f the gas exchange compartment is affected structurally and functionally by pre-natal under­ nutrition.

A recent study by Mathews et al. examined the influence o f smoking status and age on nutrient intakes o f 774 women during pregnancy (Mathews et al. 2000). The authors reported that pregnant smokers had poorer intakes o f most micronutrients than non-smokers. Although some antioxidants such as zinc were consumed in similar amounts by smokers and non-smokers o f comparable age and education, the apparently greater requirement for antioxidants among smokers means that their poor

intakes may have greater biological implications. In addition, older women had higher intakes of most nutrients than younger women. Thus young smokers are at risk o f poor nutritional status during pregnancy (Mathews et al. 2000). There is however, currently no evidence that antioxidant supplementation in normal pregnancies is beneficial as placental and infant birthweights were not associated with the intake o f any micronutrient during early or late pregnancy (Mathews et al.

2000).

In a recent prospective Aberdeen study, Devereux and colleagues demonstrated that in vitro T helper cell proliferative responses o f cord blood mononuclear cells (CBMC) to allergenic stimuli from a sample o f 223 neonates, representative of children bom to a cohort of 2000 pregnant women, were positively associated with established epidemiological risk factors for asthma and atopic disease, including history o f atopy and maternal smoking (Devereux et al. 2002). In addition, the CBMC-proliferative responses were negatively associated with maternal dietary intake o f vitamin E (Devereux et al. 2002), the reduced intake o f which is being increasingly associated with atopic disease in children and adults (Bodner et al. 1999; Hijazi et al. 2000). Hence, the demonstration o f an association between maternal dietary intake of vitamin B and the development o f the fetal immune system suggests that manipulation o f maternal diet during pregnancy should be further investigated.