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The low prevalence of female smoking in the developing world: gender inequality or maternal adaptations for fetal protection?

ABSTRACT: Female smoking prevalence is dramatically lower in developing countries (3.1%) than developed countries (17.2%), whereas male smoking is similar (32% vs 30.1%). Low female smoking has been linked to high gender inequality. Alternatively, to protect their offspring from teratogenic substances, pregnant and lactating women appear to have evolved aversions to toxic plant substances like nicotine, which are reinforced by cultural proscriptions. Higher total fertility rates (TFRs) in developing countries could therefore explain their lower prevalence of female smoking.To compare the associations of TFR and gender inequality with national prevalence rates of female and male smoking.Data from a previous study of smoking prevalence vs gender inequality in 74 countries were reanalysed with a regression model that also included TFR. We replicated this analysis with three additional measures of gender equality and 2012 smoking data from 173 countries.A 1 SD increase in TFR predicted a decrease in female smoking prevalence by factors of 0.58-0.77, adjusting for covariates. TFR had a smaller and unexpected negative association with male smoking prevalence. Increased gender equality was associated with increased female smoking prevalence, and, unexpectedly, with decreased male smoking prevalence. TFR was also associated with an increase in smoking prevalence among postmenopausal women.High TFR and gender inequality both predict reduced prevalence of female smoking across nations. In countries with high TFR, adaptations and cultural norms that protect fetuses from plant toxins might suppress smoking among frequently pregnant and lactating women.

SUBMITTER: Hagen EH

PROVIDER: S-EPMC4931906 | biostudies-other | 2016

REPOSITORIES: biostudies-other

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The low prevalence of female smoking in the developing world: gender inequality or maternal adaptations for fetal protection?

Hagen Edward H EH Garfield Melissa J MJ Sullivan Roger J RJ

Evolution, medicine, and public health 20160704 1

<h4>Background</h4>Female smoking prevalence is dramatically lower in developing countries (3.1%) than developed countries (17.2%), whereas male smoking is similar (32% vs 30.1%). Low female smoking has been linked to high gender inequality. Alternatively, to protect their offspring from teratogenic substances, pregnant and lactating women appear to have evolved aversions to toxic plant substances like nicotine, which are reinforced by cultural proscriptions. Higher total fertility rates (TFRs) ...[more]

PMID: 27193200

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Project description:Maternal and infant mortality are highly devastating, yet, in many cases, preventable events for a community. The human development of a country is a strong predictor of maternal and infant mortality, reflecting the importance of socioeconomic factors in determinants of health. Previous research has shown that the Human Development Index (HDI) predicts infant mortality rate (IMR) and the maternal mortality ratio (MMR). Inequality has also been shown to be associated with worse health in certain populations. The main purpose of the present study was to determine the correlation and predictive power of the Inequality Adjusted Human Development Index (IHDI) as a measure of inequality with the Infant Mortality Rate (IMR), Maternal Mortality Rate (MMR), Early Neonatal Mortality Rate (ENMR), Late Neonatal Mortality Rate (LNMR), and the Post Neonatal Mortality Rate (PNMR).Data for the present study were downloaded from two sources: infant and maternal mortality data were downloaded from the Global Burden of Disease 2013 Cause of Death Database and the Human Development Index (HDI) and Inequality-Adjusted Human Development Index (IHDI) data were downloaded from the United Nations Development Program (UNDP). Pearson correlation coefficients were estimated, following logarithmic transformations to the data, to examine the relationship between HDI and IHDI with MMR, IMR, ENMR, LNMR, and PNMR. Steiger's Z test for the equality of two dependent correlations was utilized in order to determine whether the HDI or IHDI was more strongly associated with the outcome variables. Lastly, we constructed OLS regression models in order to determine the predictive power of the HDI and IHDI in terms of the MMR, IMR, ENMR, LNMR, and PNMR. Maternal and infant mortality were both strongly and negatively correlated with both HDI and IHDI; however, Steiger's Z test for the equality of two dependent correlations revealed that IHDI was more strongly correlated than HDI with MMR (Z = 4.897, p < 0.001), IMR (Z = 2.524, p = 0.012), ENMR (Z = 2.936, p = 0.003), LNMR (Z = 2.272, p = 0.023), and PNMR (Z = 2.277, p = 0.023). Furthermore, side-by-side OLS regression models revealed that, when IHDI was used as the predictor variable instead of HDI, the R2 value was 0.053 higher for MMR, 0.025 higher for IMR, 0.038 higher for ENMR, 0.029 higher for LNMR, and 0.026 higher for PNMR.Even when both the HDI and the IHDI correlate with the infant and maternal mortality rates, the IHDI is a better predictor for these two health indicators. Therefore, these results add more evidence that inequality is playing an important role in determining the health status of various populations in the world and more efforts should be put into programs to fight inequality.

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Project description:BackgroundMaternal smoking is a risk factor for pediatric lung disease, including asthma. Animal models suggest that maternal smoking causes defective alveolarization in the offspring. Retinoic acid signaling modulates both lung development and postnatal immune function. Thus, abnormalities in this pathway could mediate maternal smoking effects. We tested whether maternal smoking disrupts retinoic acid pathway expression and functioning in a murine model.MethodsFemale C57Bl/6 mice with/without mainstream cigarette smoke exposure (3 research cigarettes a day, 5 days a week) were mated to nonsmoking males. Cigarette smoke exposure continued throughout the pregnancy and after parturition. Lung tissue from the offspring was examined by mean linear intercept analysis and by quantitative PCR. Cell culture experiments using the type II cell-like cell line, A549, tested whether lipid-soluble cigarette smoke components affected binding and activation of retinoic acid response elements in vitro.ResultsCompared to tobacco-naïve mice, juvenile mice with tobacco toxin exposure had significantly (P < 0.05) increased mean linear intercepts, consistent with an alveolarization defect. Tobacco toxin exposure significantly (P < 0.05) decreased mRNA and protein expression of retinoic acid signaling pathway elements, including retinoic acid receptor alpha and retinoic acid receptor beta, with the greatest number of changes observed between postnatal days 3-5. Lipid-soluble cigarette smoke components significantly (P < 0.05) decreased retinoic acid-induced binding and activation of the retinoic acid receptor response element in A549 cells.ConclusionsA murine model of maternal cigarette smoking causes abnormal alveolarization in association with altered retinoic acid pathway element expression in the offspring. An in vitro cell culture model shows that lipid-soluble components of cigarette smoke decrease retinoic acid response element activation. It is feasible that disruption of retinoic acid signaling contributes to the pediatric lung dysfunction caused by maternal smoking.

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The low prevalence of female smoking in the developing world: gender inequality or maternal adaptations for fetal protection?

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The low prevalence of female smoking in the developing world: gender inequality or maternal adaptations for fetal protection?

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