Related Articles Caffeine intake and small-for-gestational-age birth: modifying effects of xenobiotic-metabolising genes and smoking. Paediatr Perinat Epidemiol. 2007 Jul;21(4):300-9 Authors: Infante-Rivard C The relationship between caffeine consumption and small-for-gestational-age (SGA) birth remains uncertain. However, factors that can influence caffeine metabolism, such as genetic polymorphisms, have not been considered, while other similar factors such as smoking and ethnicity have not always been fully accounted for in the interpretation of results. A case-control study was carried out comprising 493 cases and 472 controls. Cases were newborns whose birthweight was below the 10th percentile according to gestational age and sex, based on national norms, and controls were at or above the 10th percentile. Caffeine consumption from beverages was estimated for each pregnancy trimester. Maternal and newborn variants in the CYP1A2 and CYP2E1 genes involved in the metabolism of caffeine were determined. Contrasting consumption >/=300 mg/day with a lower level, or using caffeiwne as a continuous measure, while adjusting for smoking and nausea, showed no increased risk for SGA. However, when stratifying for cigarette smoking, caffeine odds ratios (for the continuous and dichotomous measures) in the first trimester were statistically heterogeneous, suggesting a greater risk among non-smokers. Using birthweight as the outcome and caffeine as a continuous measure, a small 38 g [95% confidence interval -68, -8] decrement for every 100 mg of daily caffeine was observed in the third trimester. The studied polymorphisms did not modify the effect of caffeine. Caffeine consumption is unlikely to be a major risk factor for SGA or low birthweight in pregnant women.
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Related Articles Excess Transmission of the NAD(P)H:Quinone Oxidoreductase 1 (NQO1) C609T Polymorphism in Families of Children with Acute Lymphoblastic Leukemia. Am J Epidemiol. 2007 Mar 1; Authors: Infante-Rivard C, Vermunt JK, Weinberg CR Topoisomerase II is a DNA-processing enzyme, and secondary acute myeloid leukemia has been associated with exposure to drugs that inhibit its action. Hence, prenatal exposure to chemicals that inhibit topoisomerase II could plausibly contribute to the incidence of childhood leukemia. The NAD(P)H:quinone oxidoreductase 1 (NQO1) enzyme is involved in the metabolism of topoisomerase II-inhibiting chemicals. A functional polymorphism (C609T) associated with reduced activity has been identified on the NQO1 gene. To assess its role in the etiology of childhood acute lymphoblastic leukemia, the authors studied transmission of the variant T allele in the families (parents and grandparents) of 657 affected children in Québec, Canada (1980-2000). Log-linear models that stratified on parental or grandparental mating types were used. Prenatal exposure to potential topoisomerase II inhibitors such as benzene and maternal smoking was studied, as well as interactions between the variant and these exposures. The variant allele was transmitted to cases more frequently than expected (for one or two copies of the allele vs. none, relative risk = 1.39, 95% confidence interval: 1.07, 1.79). There was no evidence of a maternally mediated genetic effect on risk, based on a log-linear assessment of genetic symmetry between mothers and fathers, nor was there evidence of interaction between the studied maternal exposures and the child or maternal variant.
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Related Articles Indoor ultrafine particle exposures and home heating systems: A cross-sectional survey of Canadian homes during the winter months. J Expo Sci Environ Epidemiol. 2006 Oct 11; Authors: Weichenthal S, Dufresne A, Infante-Rivard C, Joseph L Exposure to airborne particulate matter has a negative effect on respiratory health in both children and adults. Ultrafine particle (UFP) exposures are of particular concern owing to their enhanced ability to cause oxidative stress and inflammation in the lungs. In this investigation, our objective was to examine the contribution of home heating systems (electric baseboard heaters, wood stoves, forced-air oil/natural gas furnace) to indoor UFP exposures. We conducted a cross-sectional survey in 36 homes in the cities of Montréal, Québec, and Pembroke, Ontario. Real-time measures of indoor UFP concentrations were collected in each home for approximately 14 h, and an outdoor UFP measurement was collected outside each home before indoor sampling. A home-characteristic questionnaire was also administered, and air exchange rates were estimated using carbon dioxide as a tracer gas. Average UFP exposures of 21,594 cm(-3) (95% confidence interval (CI): 14,014, 29,174) and 6660 cm(-3) (95% CI: 4339, 8982) were observed for the evening (1600-2400) and overnight (2400-0800) hours, respectively. In an unadjusted comparison, overnight baseline UFP exposures were significantly greater in homes with electric baseboard heaters as compared to homes using forced-air oil or natural gas furnaces, and homes using wood stoves had significantly greater overnight baseline UFP exposures than homes using forced-air natural gas furnaces. However, in multivariate models, electric oven use (beta=12,253 cm(-3), 95% CI: 3524, 20,982), indoor relative humidity (beta=1136 cm(-3) %, 95% CI: 372, 1899), and indoor smoking (beta=18,192 cm(-3), 95% CI: 2073, 34,311) were the only significant determinants of mean indoor UFP exposure, whereas air exchange rate (beta=4351 cm(-3) h(-1), 95% CI: 1507, 7195) and each 10,000 cm(-3) increase in outdoor UFPs (beta=811 cm(-3), 95% CI: 244,1377) were the only significant determinants of overnight baseline UFP exposures. In general, our findings suggest that home heating systems are not important determinants of indoor UFP exposures.Journal of Exposure Science and Environmental Epidemiology advance online publication, 11 October 2006; doi:10.1038/sj.jes.7500534.
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