Exposure to Oxidized Nitrogen: Lipid Peroxidation and Neonatal Health Risk

Tabacova, Sonia; Baird, Donna D.; Balabaeva, Liudmila

doi:10.1080/00039899809605698

Cited by 45 publications

(28 citation statements)

References 18 publications

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“…Increased lipidic peroxidation in the maternal or foetal compartment has been associated to prematurity. It has been observed in experimental studies that NO 2 during pregnancy induces lipid peroxidation in the placenta, high post-implantation embryonic lethality, and disturbances of postnatal development [36]. (7) The pathogenesis of IUGR is produced by an abnormal reaction between the trophoblast and the uterine tissues within the first weeks of gestation, therefore, an alteration of growth may result from a suboptimal placentation and maternal hemodynamic maladaptation [37] which could be due to exposure to air pollutants during the first month of gestation [3].…”

Section: Resultsmentioning

confidence: 99%

Exposure to ambient air pollution and prenatal and early childhood health effects

2005

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Over the last years, concern for the possible influence of exposure to air pollutants in children during gestation or the first years of life has grown; exposure levels which may be reached nowadays in our dwellings and in our streets. In the present study evidence over the possible impact of ambient air pollution on the foetus and the infants (i.e.: less than 1 year) published during the last decade, 1994--2003, are revised. Studies on infant mortality and exposure to particles show an outstanding consistence in the magnitude of the effects, despite the different designs used. As a whole, data show that an increase in 10 microg/m3 of particle concentration (measured as PM10) is associated with to about 5% increase in post-neonatal mortality for all causes and around 22% for post-neonatal mortality for respiratory diseases. Regarding damage in foetal health, although results are not always consistent, most studies show associations with exposure to air pollution during pregnancy. However, the precise mechanisms of action of air pollutants on adverse reproductive results are still unknown, so is the period of exposure most relevant during pregnancy and the specific pollutant which may represent a higher risk. Follow-up studies evaluating personal exposure to different air pollutants are required, allowing for the adequate evaluation of the impact of each pollutant in different periods of pregnancy, as well as providing hypotheses on their possible mechanisms of action.

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Section: Resultsmentioning

confidence: 99%

Exposure to ambient air pollution and prenatal and early childhood health effects

2005

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“…Exposure to NO 2 during pregnancy is associated with an increased lipid peroxidation in the placenta, elevated postimplantation embryonic lethality, and disturbances of postnatal development (Tabacova et al, 1998). It has also been demonstrated that maternal exposure to NO 2 can increase the risk of pregnancy complications as a consequence of initiation of the formation of cell-damaging lipid peroxides and a decrease in maternal antioxidant reserves (Tabacova et al, 1998). Moison et al (1993) found that an increased lipid peroxidation of surfactants in maternal or fetal tissue compartments has been associated with preterm birth.…”

Section: Discussionmentioning

confidence: 99%

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction

Liu

Krewski

Shi

et al. 2006

J Expo Sci Environ Epidemiol

109

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Previous research demonstrated consistent associations between ambient air pollution and emergency room visits, hospitalizations, and mortality. Effect of air pollution on perinatal outcomes has recently drawn more attention. We examined the association between intrauterine growth restriction (IUGR) among singleton term live births and sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), carbon monoxide (CO), ozone (O 3 ), and fine particles (PM 2.5 ) present in ambient air in the Canadian cities of Calgary, Edmonton, and Montreal for the period 1985-2000. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for IUGR, based on average daily levels of individual pollutants over each month and trimester of pregnancy after adjustment for maternal age, parity, infant gender, season, and city of residence. A 1 ppm increase in CO was associated with an increased risk of IUGR in the first (OR ¼ 1.18; 95% CI 1.14-1.23), second (OR ¼ 1.15; 95% CI 1.10-1.19) and third (OR ¼ 1.19; 95% CI 1.14-1.24) trimesters of pregnancy, respectively. A 20 ppb increase in NO 2 (OR ¼ 1.16; 95% CI 1.09-1.24; OR ¼ 1.14; 95% CI 1.06-1.21; and OR ¼ 1.16; 95% CI 1.09-1.24 in the first, second, and third trimesters) and a 10 mg/m 3 increase in PM 2.5 (OR ¼ 1.07; 95% CI 1.03-1.10; OR ¼ 1.06; 95% CI 1.03-1.10; and OR ¼ 1.06; 95% CI 1.03-1.10) were also associated with an increased risk of IUGR. Consistent results were found when ORs were calculated by month rather than trimester of pregnancy. Our findings add to the emerging body of evidence that exposure to relatively low levels of ambient air pollutants in urban areas during pregnancy is associated with adverse effects on fetal growth.

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“…Tabacova et al [56] have documented the involvement of oxidative stress in the pathogenesis of adverse prenatal effects associated with exposure to oxidized nitrogen compounds. Pregnant women exposed to extensive environmental contamination by oxidized nitrogen compounds were studied at parturition and their neonatal health status was assessed.…”

Section: Exposure To Oxidized Nitrogen Species (Toxic Substances) Andmentioning

confidence: 99%

Causes of Oxidative Stress in the Pre- and Perinatal Period

et al. 2002

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Oxidative stress may be defined as an imbalance between pro-oxidant and antioxidant forces resulting in an overall pro-oxidant insult. Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, augmented levels of oxidative stress would be expected. Arguments for a role of oxidative stress/oxidative lipid derivatives in the pathogenesis of preeclampsia are documented in many papers and evidence continues to accumulate that oxidative stress is a mediator of endothelial dysfunction and thus contributes to the cardiovascular complications of preeclampsia. Also other conditions, such as toxic substance exposure, smoking and asphyxia likewise induce oxidative stress. The oxidized lipid products generated as a consequence of these conditions are highly reactive and cause damage to cells and cell membranes. Thus, increased oxidative stress accompanied by reduced endogenous defences may play a role in the pathogenesis of a number of diseases in the newborn.

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Exposure to Oxidized Nitrogen: Lipid Peroxidation and Neonatal Health Risk

Cited by 45 publications

References 18 publications

Exposure to ambient air pollution and prenatal and early childhood health effects

Exposure to ambient air pollution and prenatal and early childhood health effects

Association between maternal exposure to ambient air pollutants during pregnancy and fetal growth restriction

Causes of Oxidative Stress in the Pre- and Perinatal Period

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