Environmental Exposures, Genetic Susceptibility and Preterm Birth

Preterm births cause a large public-health burden because of its high prevalence, leading cause of neonatal morbidity and mortality, and environmental hazards is considered to be a potential risk factors (Adams et al., 2000; Bloom et al., 2001; Tucker & McGuire, 2004; Colvin et al. 2004; Fraser et al. 2004; Murphy et al. 2004). The frequency of preterm births is about 12–13% in the USA and 5–9% in many other developed countries; however, the rate of preterm birth has increased in many locations (Goldenberg et al., 2008). Thus, to elicit of risk factors that could predict high risk of preterm birth represents a challenge to practitioners and researchers. The increasing rate of preterm birth in recent decades, despite improvements in health care, creates an impetus to better understand and prevent this disorder. The identification of women at increased risk of preterm delivery is an important challenge. Preterm birth likely depends on a number of interacting factors, including genetic, epigenetic, and environmental risk factors (Windham et al., 2000; Plunkett & Muglia, 2008). The epidemiological data suggested that both genetic factors and socioenvironmental factors may influence preterm birth (Wang et al., 2000; Nukui et al., 2004; Lewis et al., 2006; Suh et al., 2008)Aplinkotyros katedraVytauto Didžiojo universiteta

Individual exposures to drinking water trihalomethanes, low birth weight and small for gestational age risk: a prospective Kaunas cohort study

<p>Abstract</p> <p>Background</p> <p>Evidence for an association between exposure during pregnancy to trihalomethanes (THMs) in drinking water and impaired fetal growth is still inconsistent and inconclusive, in particular, for various exposure routes. We examined the relationship of individual exposures to THMs in drinking water on low birth weight (LBW), small for gestational age (SGA), and birth weight (BW) in singleton births.</p> <p>Methods</p> <p>We conducted a cohort study of 4,161 pregnant women in Kaunas (Lithuania), using individual information on drinking water, ingestion, showering and bathing, and uptake factors of THMs in blood, to estimate an internal dose of THM. We used regression analysis to evaluate the relationship between internal THM dose and birth outcomes, adjusting for family status, education, smoking, alcohol consumption, body mass index, blood pressure, ethnic group, previous preterm, infant gender, and birth year.</p> <p>Results</p> <p>The estimated internal dose of THMs ranged from 0.0025 to 2.40 mg/d. We found dose-response relationships for the entire pregnancy and trimester-specific THM and chloroform internal dose and risk for LBW and a reduction in BW. The adjusted odds ratio for third tertile vs. first tertile chloroform internal dose of entire pregnancy was 2.17, 95% CI 1.19-3.98 for LBW; the OR per every 0.1 μg/d increase in chloroform internal dose was 1.10, 95% CI 1.01-1.19. Chloroform internal dose was associated with a slightly increased risk of SGA (OR 1.19, 95% CI 0.87-1.63 and OR 1.22, 95% CI 0.89-1.68, respectively, for second and third tertile of third trimester); the risk increased by 4% per every 0.1 μg/d increase in chloroform internal dose (OR 1.04, 95% CI 1.00-1.09).</p> <p>Conclusions</p> <p>THM internal dose in pregnancy varies substantially across individuals, and depends on both water THM levels and water use habits. Increased internal dose may affect fetal growth.</p