05 fmh023 Mukhopadhyay (k)

biological variation within the world’s populations has been explained largely on the basis of genetic or racial differences. During the last decade or so, however, research and thinking across the world have focused on studying environmental (and potentially removable) causal mechanisms that could underlie these growth differences and differences in patterns of disease. This research has already been successful in defining a number of underlying mechanisms that could explain the differences in phenotype observed between the world’s populations. The paper by Glew, et al. in this issue addresses this theme in relation to the lung function shortfall for African racial groups compared with Caucasian racial groups. As the first step, the authors define lung function in rural and urban Nigerian children. Secondly, they compare lung function in Nigerian children with that of African-American and Caucasian children. Finally, the authors explore the hypothesis that differences in nutritional status and body composition could relate to pulmonary function in the Nigerian children. The findings are important to our understanding of the variation in lung function within the world’s populations, and the mechanisms underlying such variation. The authors show that there is a significant shortfall in lung function in Nigerian children compared with Caucasian children. However low, lung function in Nigerian children is comparable with African-American children. Urban Nigerian girls have a mean peak flow that is 20 per cent less than African-American and 32 per cent less than Caucasian standards. Are these differences a reflection of genetically determined variation in lung shape or size leading to lower or higher lung function, or the result of environmental influences, possibly acting over generations, leading to significant lung function differences between the world populations? Evidence from the Chinese would suggest the latter. Thus, while lung function in children of Chinese origin in mainland China and in Malaysia is low, lung function in the Chinese children in Singapore is much higher, compared with British Caucasian values, mirroring large GDP per capita differences between the two areas. Although other confounding factors may be responsible, the health status of the African-American community remains poor and this could be reflected in their failure to show a ‘catch-up’ (as for the Singaporean Chinese) compared with lung function in native Africans. If lung growth improves over time in association with an improvement in living standards, lung function and, in particular, lung function ‘shortfall’, could be expected to show strong associations with nutritional indices. This was observed in our work with rural Indian children. We screened 810 children (Medinipur district, West Bengal) to identify a population of 391 children with no history or physical signs of asthma and other respiratory problems. Mean forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1) were 22–32 per cent below mean Caucasian values. Furthermore, both lung function in the Indian children and the differences in lung function between Indian and Caucasian children were strongly correlated with body mass index, an indicator of nutritional status. Small lung function differences (around 3 per cent) have significant public health implications, while a 5–10 per cent lower peak FEV1 at age 20 years could increase the risk of chronic obstructive pulmonary disease in later life. The 20–30 per cent differences in lung function observed by Glew, et al. and by ourselves are thus likely to lead to major, as yet unexplored, effects on quality-of-life, economic productivity, and social (dis)advantage in these children. However, the hypothesis that environmental (and potentially removable) causal mechanisms could underlie growth differences and differences in patterns of disease between populations is currently being studied at a more general level than lung function alone. Research over the last decade has established that birthweight differences are associated with greatly altered risks of coronary heart disease, stroke, hypertension, and non-insulin dependent diabetes. Birthweight differences between populations are now known to be likely contributors to long-term disease. Both ethnicity and race are poorly defined biological entities and the evidence that biological variation is caused by ‘ethnic’ differences is weak and inconclusive. Almost as much biological variation exists within as between ‘racial’ or ‘ethnic’ groups. Gene clusters controlling drug metabolism are independent of commonly used ethnic or geographical maps. Ethnicity per se is thus unlikely to act as a significant contributory factor influencing these population differences.