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BackgroundAlthough urban residence is consistently identified as one of the primary correlates of non-communicable disease in low- and middle-income countries, it is not clear why or how urban settings predispose individuals and populations to non-communicable disease (NCD), or how this relationship could be modified to slow the spread of NCD. The urban–rural dichotomy used in most population health research lacks the nuance and specificity necessary to understand the complex relationship between urbanicity and NCD risk. Previous studies have developed and validated quantitative tools to measure urbanicity continuously along several dimensions but all have been isolated to a single country. The purposes of this study were 1) To assess the feasibility and validity of a multi-country urbanicity scale; 2) To report some of the considerations that arise in applying such a scale in different countries; and, 3) To assess how this scale compares with previously validated scales of urbanicity.MethodsHousehold and community-level data from the Young Lives longitudinal study of childhood poverty in 59 communities in Ethiopia, India and Peru collected in 2006/2007 were used. Household-level data include parents’ occupations and education level, household possessions and access to resources. Community-level data include population size, availability of health facilities and types of roads. Variables were selected for inclusion in the urbanicity scale based on inspection of the data and a review of literature on urbanicity and health. Seven domains were constructed within the scale: Population Size, Economic Activity, Built Environment, Communication, Education, Diversity and Health Services.ResultsThe scale ranged from 11 to 61 (mean 35) with significant between country differences in mean urbanicity; Ethiopia (30.7), India (33.2), Peru (39.4). Construct validity was supported by factor analysis and high corrected item-scale correlations suggest good internal consistency. High agreement was observed between this scale and a dichotomized version of the urbanicity scale (Kappa 0.76; Spearman’s rank-correlation coefficient 0.84 (p < 0.0001). Linear regression of socioeconomic indicators on the urbanicity scale supported construct validity in all three countries (p < 0.05).ConclusionsThis study demonstrates and validates a robust multidimensional, multi-country urbanicity scale. It is an important step on the path to creating a tool to assess complex processes like urbanization. This scale provides the means to understand which elements of urbanization have the greatest impact on health.

Diethylhexylphthalate (DEHP) and diisononylphthalate (DINP) are plasticizers with many important commercial, industrial and medical applications. However, both DEHP and DINP are rodent peroxisome proliferators (PPs), a class of compounds that cause rodent liver tumours associated with peroxisome proliferation, induction of hepatic DNA synthesis and the suppression of apoptosis. Despite these effects in the rodent, humans appear to be nonresponsive to the adverse effects of PPs. Previously, we have shown that the fibrate hypolipidaemic peroxisome proliferator, nafenopin, induced DNA synthesis and suppressed apoptosis in rat but not in human hepatocytes. In this work, we have examined species differences in the response of rat and human hepatocytes to DEHP and DINP in vitro. In rat hepatocytes in vitro, both DINP and MEHP (a principle metabolite of DEHP and the proximal peroxisome proliferator) caused a concentration-dependent induction of DNA synthesis and suppression of both spontaneous and transforming growth factor beta1 (TGFbeta1)-induced apoptosis. Similarly, both MEHP and DINP caused a concentration-dependent induction of peroxisomal beta-oxidation although the response to DINP was less robust. In contrast to the pleiotropic response noted in rat hepatocytes, neither DINP nor MEHP caused an induction of beta-oxidation, stimulation of DNA synthesis and suppression of apoptosis in human hepatocytes cultured from three separate donors. These data provide evidence for species differences in the hepatic response to the phthalates DEHP and DINP, confirming that human hepatocytes appear to be refractory to the hepatocarcinogenic effects of PPs first noted in rodents.

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