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Ambient Air Pollution Exposure and Fecundability in Women Undergoing In Vitro Fertilization.

ABSTRACT: Background:Limited research suggests ambient air pollution impairs fecundity but groups most susceptible have not been identified. We studied whether long-term ambient air pollution exposure prior to an in vitro fertilization (IVF) cycle was associated with successful livebirth, and whether associations were modified by underlying infertility diagnosis. Methods:Data on women initiating their 1st autologous IVF cycle in 2012-13 were obtained from four U.S. clinics. Outcomes included pregnancy, pregnancy loss, and livebirth. Annual average exposure to fine particulate matter (PM2.5), PM10, and nitrogen dioxide (NO2) prior to IVF start were estimated at residential address using a validated national spatial model incorporating land-use regression and universal kriging. We also assessed residential distance to major roadway. We calculated risk ratios (RR) using modified Poisson regression and evaluated effect modification (EM) by infertility diagnosis on additive and multiplicative scales. Results:Among 7,463 eligible participants, 36% had a livebirth. There was a non-significant indication of an association between PM2.5 or NO2 and decreased livebirth and increased pregnancy loss. Near roadway residence was associated with decreased livebirth (RR: 0.96, 95% CI: 0.82, 0.99. There was evidence for EM between high exposure to air pollutants and a diagnosis of diminished ovarian reserve (DOR) or male infertility and decreased livebirth. Conclusions:Despite suggestive but uncertain findings for the overall effect of air pollution on fecundity, we found a suggestive indication that there may be synergistic effects of air pollution and DOR or male infertility diagnosis on livebirth. This suggests two possible targets for future research and intervention.

SUBMITTER: Quraishi SM

PROVIDER: S-EPMC6581510 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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Ambient Air Pollution Exposure and Fecundability in Women Undergoing In Vitro Fertilization.

Quraishi Sabah M SM Lin Paul C PC Richter Kevin S KS Hinckley Mary D MD Yee Bill B Neal-Perry Genevieve G Sheppard Lianne L Kaufman Joel D JD Hajat Anjum A

Environmental epidemiology (Philadelphia, Pa.) 20190201 1

<h4>Background</h4>Limited research suggests ambient air pollution impairs fecundity but groups most susceptible have not been identified. We studied whether long-term ambient air pollution exposure prior to an in vitro fertilization (IVF) cycle was associated with successful livebirth, and whether associations were modified by underlying infertility diagnosis.<h4>Methods</h4>Data on women initiating their 1<sup>st</sup> autologous IVF cycle in 2012-13 were obtained from four U.S. clinics. Outco ...[more]

PMID: 31214664

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Project description:Accumulating evidence suggests that air pollution increases pregnancy loss; however, most previous studies have focused on case identification from medical records, which may underrepresent early pregnancy losses. Our objective was to investigate the association between acute and chronic exposure to ambient air pollution and time to pregnancy loss among women undergoing assisted reproductive technologies (ART) who are closely followed throughout early pregnancy. We included 275 women (345 human chorionic gonadotropin (hCG)-confirmed pregnancies) undergoing ART at a New England academic fertility center. We estimated daily nitrogen dioxide (NO2), ozone (O3), fine particulate matter <2.5 μm (PM2.5), and black carbon (BC) exposures using validated spatiotemporal models estimated from first positive hCG test until day of failure or live birth. Air pollution exposures were averaged over the past week and the whole pregnancy. Multivariable Cox proportional hazards models were used to estimate the hazards ratio (HR) for pregnancy loss for an interquartile range (IQR) increase in pollutant exposure. We tested for violation of proportional hazards by considering an interaction between time (in days) since positive hCG (<30 days vs. ≥30 days) and air pollution. The incidence of pregnancy loss was 29 per 100 confirmed pregnancies (n = 99). Among pregnancies not resulting in live birth, the median (IQR) time to loss was 21 (11, 30) days following positive hCG. Average past week exposures to NO2, O3, PM2.5, and BC were not associated with time to pregnancy loss. Exposure throughout pregnancy to NO2 was not associated with pregnancy loss; however, there was a statistically significant interaction with time (p-for-interaction<0.001). Specifically, an IQR increase in exposure to NO2 was positively associated with pregnancy loss after 30 days (HR = 1.34, 95% CI: 1.13, 1.58), but not in the first 30 days after positive hCG (HR = 0.83, 95% CI: 0.57, 1.20). Overall pregnancy exposure to O3, PM2.5, and BC were not associated with pregnancy loss regardless of timing. Models evaluating joint effects of all pollutants yielded similar findings. In conclusion, acute and chronic exposure to NO2, O3, PM2.5, and BC were not associated with risk of pregnancy loss; however, higher exposure to NO2 throughout pregnancy was associated with increased risk of loss 30 days after positive hCG. In this cohort, later pregnancy losses appeared more susceptible to the detrimental effects of air pollution exposure.

Project description:STUDY QUESTION:Does ambient air pollution affect fecundability? SUMMARY ANSWER:While cycle-average air pollution exposure was not associated with fecundability, we observed some associations for acute exposure around ovulation and implantation with fecundability. WHAT IS KNOWN ALREADY:Ambient air pollution exposure has been associated with adverse pregnancy outcomes and decrements in semen quality. STUDY DESIGN, SIZE, DURATION:The LIFE study (2005-2009), a prospective time-to-pregnancy study, enrolled 501 couples who were followed for up to one year of attempting pregnancy. PARTICIPANTS/MATERIALS, SETTING, METHODS:Average air pollutant exposure was assessed for the menstrual cycle before and during the proliferative phase of each observed cycle (n = 500 couples; n = 2360 cycles) and daily acute exposure was assessed for sensitive windows of each observed cycle (n = 440 couples; n = 1897 cycles). Discrete-time survival analysis modeled the association between fecundability and an interquartile range increase in each pollutant, adjusting for co-pollutants, site, age, race/ethnicity, parity, body mass index, smoking, income and education. MAIN RESULTS AND THE ROLE OF CHANCE:Cycle-average air pollutant exposure was not associated with fecundability. In acute models, fecundability was diminished with exposure to ozone the day before ovulation and nitrogen oxides 8 days post ovulation (fecundability odds ratio [FOR] 0.83, 95% confidence interval [CI]: 0.72, 0.96 and FOR 0.84, 95% CI: 0.71, 0.99, respectively). However, particulate matter ≤10 microns 6 days post ovulation was associated with greater fecundability (FOR 1.25, 95% CI: 1.01, 1.54). LIMITATIONS, REASONS FOR CAUTION:Although our study was unlikely to be biased due to confounding, misclassification of air pollution exposure and the moderate study size may have limited our ability to detect an association between ambient air pollution and fecundability. WIDER IMPLICATIONS OF THE FINDINGS:While no associations were observed for cycle-average ambient air pollution exposure, consistent with past research in the United States, exposure during critical windows of hormonal variability was associated with prospectively measured couple fecundability, warranting further investigation. STUDY FUNDING/COMPETING INTEREST(S):This work was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (Longitudinal Investigation of Fertility and the Environment study contract nos. #N01-HD-3-3355, NO1-HD-#-3356, N01-HD-3-3358 and the Air Quality and Reproductive Health Study Contract No. HHSN275200800002I, Task Order No. HHSN27500008). We declare no conflict of interest.

Project description:BackgroundOlfactory dysfunction affects millions of people worldwide. This sensory impairment is associated with neurodegenerative disease and significantly decreased quality of life. Exposure to airborne pollutants has been implicated in olfactory decline, likely due to the anatomic susceptibility of the olfactory nerve to the environment. Historically, studies have focused on occupational exposures, but more recent studies have considered effects from exposure to ambient air pollutants.ObjectivesTo examine all relevant human data evaluating a link between ambient pollution exposure and olfaction and to review supporting animal data in order to examine potential mechanisms for pollution-associated olfactory loss.MethodsWe identified and reviewed relevant articles from 1950 to 2015 using PubMed and Web of Science and focusing on human epidemiologic and pathophysiologic studies. Animal studies were included only to support pertinent data on humans. We reviewed findings from these studies evaluating a relationship between environmental pollutant exposure and olfactory function.ResultsWe identified and reviewed 17 articles, with 1 additional article added from a bibliography search, for a total of 18 human studies. There is evidence in human epidemiologic and pathologic studies that increased exposure to ambient air pollutants is associated with olfactory dysfunction. However, most studies have used proxies for pollution exposure in small samples of convenience. Human pathologic studies, with supporting animal work, have also shown that air pollution can contact the olfactory epithelium, translocate to the olfactory bulb, and migrate to the olfactory cortex. Pollutants can deposit at each location, causing direct damage and disruption of tissue morphology or inducing local inflammation and cellular stress responses.ConclusionsAmbient air pollution may impact human olfactory function. Additional studies are needed to examine air pollution-related olfactory impacts on the general population using measured pollution exposures and to link pollution exposure with olfactory dysfunction and related pathology. Citation: Ajmani GS, Suh HH, Pinto JM. 2016. Effects of ambient air pollution exposure on olfaction: a review. Environ Health Perspect 124:1683-1693; http://dx.doi.org/10.1289/EHP136.

Project description:BackgroundStudies have identified relationships between air pollution and birth weight, but have been inconsistent in identifying individual pollutants inversely associated with birth weight or elucidating susceptibility of the fetus by trimester of exposure. We examined effects of prenatal ambient pollution exposure on average birth weight and risk of low birth weight in full-term births.MethodsWe estimated average ambient air pollutant concentrations throughout pregnancy in the neighborhoods of women who delivered term singleton live births between 1996 and 2006 in California. We adjusted effect estimates of air pollutants on birth weight for infant characteristics, maternal characteristics, neighborhood socioeconomic factors, and year and season of birth.Results3,545,177 singleton births had monitoring for at least one air pollutant within a 10 km radius of the tract or ZIP Code of the mother's residence. In multivariate models, pollutants were associated with decreased birth weight; -5.4 grams (95% confidence interval -6.8 g, -4.1 g) per ppm carbon monoxide, -9.0 g (-9.6 g, -8.4 g) per pphm nitrogen dioxide, -5.7 g (-6.6 g, -4.9 g) per pphm ozone, -7.7 g (-7.9 g, -6.6 g) per 10 microg/m3 particulate matter under 10 microm, -12.8 g (-14.3 g, -11.3 g) per 10 microg/m3 particulate matter under 2.5 microm, and -9.3 g (-10.7 g, -7.9 g) per 10 microg/m3 of coarse particulate matter. With the exception of carbon monoxide, estimates were largely unchanged after controlling for co-pollutants. Effect estimates for the third trimester largely reflect the results seen from full pregnancy exposure estimates; greater variation in results is seen in effect estimates specific to the first and second trimesters.ConclusionsThis study indicates that maternal exposure to ambient air pollution results in modestly lower infant birth weight. A small decline in birth weight is unlikely to have clinical relevance for individual infants, and there is debate about whether a small shift in the population distribution of birth weight has broader health implications. However, the ubiquity of air pollution exposures, the responsiveness of pollutant levels to regulation, and the fact that the highest pollution levels in California are lower than those regularly experienced in other countries suggest that precautionary efforts to reduce pollutants may be beneficial for infant health from a population perspective.

Project description:Objectives: Exposure to air pollutants has been linked to preterm birth (PTB) after natural conception. However, few studies have explored the effects of air pollution on PTB in patients who underwent in vitro fertilization (IVF). We aimed to investigate the association between ambient air pollutants exposure and PTB risk in IVF patients. Methods: This retrospective cohort study included 2,195 infertile women who underwent IVF treatment from January 2017 and September 2020 in Hangzhou Women's Hospital. Totally 1,005 subjects who underwent a first fresh embryo(s) transfer cycle were analyzed in this study. Residential exposure to ambient six air pollutants (PM2.5, PM10, SO2, NO2, CO, O3) during various periods of the IVF timeline were estimated by satellite remote-sensing and ground measurement. Cox proportional hazards models for discrete time were used to explore the association between pollutants exposure and incident PTB, with adjustment for confounders. Stratified analyses were employed to explore the effect modifiers. Results: The clinical pregnancy and PTB rates were 61.2 and 9.3%, respectively. We found that PM2.5 exposure was significantly associated with an increased risk of PTB during 85 days before oocyte retrieval [period A, adjusted hazard ratio, HR=1.09, 95%CI: 1.02-1.21], gonadotropin start to oocyte retrieval [period B, 1.07 (1.01-1.19)], first trimester of pregnancy [period F, 1.06 (1.01-1.14)], and the entire IVF pregnancy [period I, 1.07 (1.01-1.14)], respectively. An interquartile range increment in PM10 during periods A and B was significantly associated with PTB at 1.15 (1.04-1.36), 1.12 (1.03-1.28), and 1.14 (1.01-1.32) for NO2 during period A. The stratified analysis showed that the associations were stronger for women aged <35 years and those who underwent two embryos transferred. Conclusions: Our study suggests ambient PM2.5, PM10, and NO2 exposure were significantly associated with elevated PTB risk in IVF patients, especially at early stages of IVF cycle and during pregnancy.

Project description:BACKGROUND:A few studies suggest that air pollution may decrease fertility, but prospective studies and examinations of windows of susceptibility remain unclear. OBJECTIVE:We aimed to examine the association between time-varying exposure to nitrogen dioxide ([Formula: see text]), ozone ([Formula: see text]), fine particulate matter [Formula: see text] ([Formula: see text]), and black carbon (BC) on in vitro fertilization (IVF) outcomes. METHODS:We included 345 women (522 IVF cycles) for the [Formula: see text], [Formula: see text], and [Formula: see text] analyses and 339 women (512 IVF cycles) for the BC analysis enrolled in a prospective cohort at a Boston fertility center (2004–2015). We used validated spatiotemporal models to estimate daily residential exposure to [Formula: see text], [Formula: see text], [Formula: see text], and BC. Multivariable discrete time Cox proportional hazards models with four periods [ovarian stimulation (OS), oocyte retrieval to embryo transfer (ET), ET to implantation, implantation to live birth] estimated odds ratios (OR) and 95% confidence intervals (CI) of failing at IVF. Time-dependent interactions were used to identify vulnerable periods. RESULTS:An interquartile range (IQR) increase in [Formula: see text], [Formula: see text], and BC throughout the IVF cycle was associated with an elevated odds of failing at IVF prior to live birth ([Formula: see text], 95% CI: 0.95, 1.23 for [Formula: see text]; [Formula: see text], 95% CI: 0.88, 1.28 for [Formula: see text]; and [Formula: see text], 95% CI: 0.96, 1.41 for BC). This relationship significantly varied across the IVF cycle such that the association with higher exposure to air pollution during OS was strongest for early IVF failures. An IQR increase in [Formula: see text], [Formula: see text], and BC exposure during OS was associated with 1.42 (95% CI: 1.20, 1.69), 1.26 (95% CI: 0.96, 1.67), and 1.23 (95% CI: 0.96, 1.59) times the odds of failing prior to oocyte retrieval, and 1.32 (95% CI: 1.13, 1.54), 1.27 (95% CI: 0.98, 1.65), and 1.32 (95% CI: 1.10, 1.59) times the odds of failing prior to ET. CONCLUSION:Increased exposure to traffic-related pollutants was associated with higher odds of early IVF failure. https://doi.org/10.1289/EHP4601.

Dataset Information

Ambient Air Pollution Exposure and Fecundability in Women Undergoing In Vitro Fertilization.

Publications

Ambient Air Pollution Exposure and Fecundability in Women Undergoing In Vitro Fertilization.

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