Exposure to air pollution during different gestational phases contributes to risks of low birth weight

Lee, B. E.; Ha, Eun Hee; Park, Hyesook; Kim, Y. J.; Hong, Yun–Chul; Kim, H.; Lee, J. T.

doi:10.1093/humrep/deg102

Cited by 141 publications

(102 citation statements)

References 55 publications

(56 reference statements)

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“…*P Ͻ 0.05 was considered statistically significant. studies linking higher PM exposure to decreases in birth weight (2,19,30,35). This is confirmed in a similar study where mice were exposed to diesel exhaust during a portion of development (15).…”

Section: -Exposed Mice (B) C: End-systolic Volume (Esv) D: Enddiassupporting

confidence: 52%

“…Evidence from epidemiological studies indicates a strong association between ambient concentrations of air pollutants, including PM, and poor developmental outcomes, such as low birth weight (3,19,23) preterm birth (34,37), and intrauterine growth restriction (10,36). Animal studies have confirmed these outcomes (25,38,40,44) and shown genetic and epigenetic changes in animals maternally exposed to air pollution (32).…”

mentioning

confidence: 99%

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Early life exposure to air pollution induces adult cardiac dysfunction

Gorr

Velten²,

Nelin

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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Exposure to ambient air pollution contributes to the progression of cardiovascular disease, particularly in susceptible populations. The objective of the present study was to determine whether early life exposure to air pollution causes persistent cardiovascular consequences measured at adulthood. Pregnant FVB mice were exposed to filtered (FA) or concentrated ambient particulate matter (PM2.5) during gestation and nursing. Mice were exposed to PM2.5 at an average concentration of 51.69 μg/m3 from the Columbus, OH region for 6 h/day, 7 days/wk in utero until weaning at 3 wk of age. Birth weight was reduced in PM2.5 pups compared with FA (1.36 ± 0.12 g FA, n = 42 mice; 1.30 ± 0.15 g PM2.5, n = 67 P = 0.012). At adulthood, mice exposed to perinatal PM2.5 had reduced left ventricular fractional shortening compared with FA-exposed mice (43.6 ± 2.1% FA, 33.2 ± 1.6% PM2.5, P = 0.001) with greater left ventricular end systolic diameter. Pressure-volume loops showed reduced ejection fraction (79.1 ± 3.5% FA, 35.5 ± 9.5% PM2.5, P = 0.005), increased end-systolic volume (10.4 ± 2.5 μl FA, 39.5 ± 3.8 μl PM2.5, P = 0.001), and reduced dP/d t maximum (11,605 ± 200 μl/s FA, 9,569 ± 800 μl/s PM2.5, P = 0.05) and minimum (−9,203 ± 235 μl/s FA, −7,045 ± 189 μl/s PM2.5, P = 0.0005) in PM2.5-exposed mice. Isolated cardiomyocytes from the hearts of PM2.5-exposed mice had reduced peak shortening (%PS, 8.53 ± 2.82% FA, 6.82 ± 2.04% PM2.5, P = 0.003), slower calcium reuptake (τ, 0.22 ± 0.09 s FA, 0.26 ± 0.07 s PM2.5, P = 0.048), and reduced response to β-adrenergic stimulation compared with cardiomyocytes isolated from mice that were exposed to FA. Histological analyses revealed greater picro-sirius red-positive-stained areas in the PM2.5 vs. FA group, indicative of increased collagen deposition. We concluded that these data demonstrate the detrimental role of early life exposure to ambient particulate air pollution in programming of adult cardiovascular diseases and the potential for PM2.5 to induce persistent cardiac dysfunction at adulthood.

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Section: -Exposed Mice (B) C: End-systolic Volume (Esv) D: Enddiassupporting

confidence: 52%

mentioning

confidence: 99%

Early life exposure to air pollution induces adult cardiac dysfunction

Gorr

Velten²,

Nelin

et al. 2014

American Journal of Physiology-Heart and Circulatory Physiology

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“…438 -444 The effects of air pollution on various other birth outcomes are substantially less well established and understood. Nevertheless, there are a growing number of contemporary studies that have evaluated potential links between air pollution and birth weight, [445][446][447][448][449][450][451][452][453][454][455][456] premature birth, 449,456 -458 fetal growth, 459 -461 intrauterine mortality, 462 birth defects, 463 and lymphocyte immunophenotypes in cord and maternal blood at delivery. 464 Recent reviews of the literature dealing with air pollution and these various birth outcomes 441,442,444 generally suggest that there may be effects of ambient PM air pollution on these outcomes but that these effects are not well understood.…”

Section: Infant/birth Outcomesmentioning

confidence: 99%

Health Effects of Fine Particulate Air Pollution: Lines that Connect

Pope

Dockery²

2006

Journal of the Air & Waste Management Association

5,499

3,159

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Efforts to understand and mitigate the health effects of particulate matter (PM) air pollution have a rich and interesting history. This review focuses on six substantial lines of research that have been pursued since 1997 that have helped elucidate our understanding about the effects of PM on human health. There has been substantial progress in the evaluation of PM health effects at different time-scales of exposure and in the exploration of the shape of the concentration-response function. There has also been emerging evidence of PM-related cardiovascular health effects and growing knowledge regarding interconnected general pathophysiological pathways that link PM exposure with cardiopulmonary morbidity and mortality. Despite important gaps in scientific knowledge and continued reasons for some skepticism, a comprehensive evaluation of the research findings provides persuasive evidence that exposure to fine particulate air pollution has adverse effects on cardiopulmonary health. Although much of this research has been motivated by environmental public health policy, these results have important scientific, medical, and public health implications that are broader than debates over legally mandated air quality standards.

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“…Recent studies have further demonstrated association between ambient air pollution and adverse pregnancy outcomes, including low birth weight, preterm birth, IUGR and birth defects in China (Xu et al, 1995;Wang et al, 1997), the Czech Republic (Bobak, 2000), the United States (Ritz and Yu, 1999;Ritz et al, 2000Ritz et al, , 2002Parker et al, 2005), and Korea (Lee et al, 2003). Recent Canadian studies have also provided evidence of a negative impact of air pollution on birth outcomes (Liu et al, 2003) and respiratory health among young children (Yang et al, 2003) in Vancouver.…”

Section: Introductionmentioning

confidence: 97%

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

106

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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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Exposure to air pollution during different gestational phases contributes to risks of low birth weight

Abstract: This study suggests that exposure to CO, PM(10,) SO(2) and NO(2) during early to mid pregnancy contribute to risks for LBW.

Cited by 141 publications

References 55 publications

Early life exposure to air pollution induces adult cardiac dysfunction

Early life exposure to air pollution induces adult cardiac dysfunction

Health Effects of Fine Particulate Air Pollution: Lines that Connect

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

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