Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic.
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ABSTRACT: Background
An increasing number of studies have linked air pollution to decreased fertility. Whether this is due to an effect on ovarian reserve is unknown.Method
Our study included 632 women attending the Massachusetts General Hospital Fertility Center (2004-2015) who had a measured antral follicle count. Validated spatiotemporal models estimated daily particulate matter <2.5 µg/m (PM2.5) (based on residential address) for the 3 months before the antral follicle count. We analyzed associations with Poisson regression.Results
Every 2 µg/m increase in estimated PM2.5 exposure was associated with a -7.2% (95% confidence interval = -10.4%, -3.8%) lower antral follicle count adjusting for age, body mass index, smoking status, and year and season of the count. The association of PM2.5 with antral follicle count was stronger among women with female factor infertility (-16.3% per 2 µg/m).Conclusions
Among women from an infertility clinic, higher PM2.5 exposure was associated with lower ovarian reserve, raising concern that air pollution may accelerate reproductive aging.
SUBMITTER: Gaskins AJ
PROVIDER: S-EPMC6550330 | biostudies-literature | 2019 Jul
REPOSITORIES: biostudies-literature
Publications
Exposure to Fine Particulate Matter and Ovarian Reserve Among Women from a Fertility Clinic.
Gaskins Audrey J AJ Mínguez-Alarcón Lidia L Fong Kelvin C KC Abdelmessih Sarah S Coull Brent A BA Chavarro Jorge E JE Schwartz Joel J Kloog Itai I Souter Irene I Hauser Russ R Laden Francine F
Epidemiology (Cambridge, Mass.) 20190701 4
<h4>Background</h4>An increasing number of studies have linked air pollution to decreased fertility. Whether this is due to an effect on ovarian reserve is unknown.<h4>Method</h4>Our study included 632 women attending the Massachusetts General Hospital Fertility Center (2004-2015) who had a measured antral follicle count. Validated spatiotemporal models estimated daily particulate matter <2.5 µg/m (PM2.5) (based on residential address) for the 3 months before the antral follicle count. We analyz ...[more]
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Project description:BackgroundEmerging data suggests PM2.5 (particulate matter with aerodynamic diameter <2.5 μm) may be associated with both earlier declines in episodic memory (EM) and increased depressive symptoms in older adults. Although late-life depressive symptoms are associated with EM, no longitudinal studies have examined the inter-relationship among PM2.5, depressive symptoms and EM.MethodsOlder women (n = 2,202; aged 67-83 in 1999) enrolled in the Women's Health Initiative Study of Cognitive Aging completed up to eight annual assessments of depressive symptoms (15-item Geriatric Depression Scale) and EM (California Verbal Learning Test). A nationwide spatiotemporal model (1999-2010) was used to estimate ambient PM2.5 exposure at residential locations. Univariate and bivariate structural equation models (SEMs) for latent-change scores were used to examine how 3-year average PM2.5 preceding each assessment affects the temporal dynamics and bidirectional relations of annual changes in depressive symptoms and EM.ResultsIn univariate SEMs, one inter-quartile (4.04 μg/m3) increment of 3-year PM2.5 was significantly (p < 0.05) associated with accelerated declines in verbal learning (List A trials 1-3: β = -1.48) and free-recall memory (short-delay: β = -1.43; long-delay: β = -1.11), but not with change in depressive symptoms (β = 0.12; p = 0.71). In bivariate SEMs, significant associations were observed between PM2.5 and accelerated declines in EM measures (β = -1.44 to -0.99; p < 0.05) and between EM performance and changes in depressive symptoms (β = -0.08 to -0.05; p < 0.05), with significant indirect PM2.5 effects on changes in depressive symptoms (β = 0.08-0.10; p < 0.05). These findings were robust with adjustment for multiple demographic, lifestyle, and clinical factors, and remained after excluding subjects with dementia or mild cognitive impairment. No associations were found between PM2.5 and change in depressive symptoms or depressive symptoms and subsequent EM decline.ConclusionsFindings suggest that PM2.5 neurotoxicity may damage brain areas implicated in EM, followed by manifestation of depressive symptoms. Our data did not support depressive symptoms as the neuropsychological mediator of accelerated brain aging associated with PM2.5 exposure.
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Project description:ObjectiveTo evaluate the associations of caffeinated, alcoholic, and sweetened beverage intakes with antral follicle count (AFC), a well-accepted biomarker of ovarian reserve.DesignObservational prospective cohort study.SettingFertility center at an academic hospital.PatientsThis study includes 567 women seeking fertility care at the Massachusetts General Hospital who participated in the Environment and Reproductive Health Study.InterventionNone. Women self-reported consumption of caffeinated (coffee, tea, soda), alcoholic (wine, beer, liquor), sugar-sweetened, and artificially sweetened beverages using a validated food-frequency questionnaire.Main outcome measureAntral follicle count was assessed using a transvaginal ultrasound performed on the 3rd day of an unstimulated menstrual cycle or on the 3rd day of a progesterone withdrawal bleed.ResultsMedian (interquartile range) age and AFC were 35.0 (32.0-38.0) years and 13.0 (9.0-18.0), respectively. Median (range) intake of caffeinated, alcoholic, sugar-sweetened, and artificially sweetened beverages in servings/day were 1.08 (0-7.08), 0.35 (0-3.84), 0.04 (0-4.80), and 0.04 (0-7.50), respectively. All examined beverages were unrelated to AFC. The multivariable adjusted mean AFC (95% confidence interval) for women in the top and bottom quartiles of intake were 13.8 (13.0-14.7) and 13.8 (12.9-14.7) for caffeinated beverages; 13.8 (13.0-14.7) and 13.8 (13.0-14.6) for alcoholic beverages; 13.5 (12.6-14.4) and 13.3 (12.4-14.2) for sugar-sweetened beverages; and 13.2 (12.4-14.1) and 13.4 (12.6-14.3) for artificially sweetened beverages.ConclusionLow-to-moderate intakes of caffeinated, alcoholic, sugar-sweetened, and artificially sweetened beverages were unrelated to ovarian reserve, as measured by AFC, in a cohort of women seeking fertility care.
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Project description:ObjectiveTo examine the association between dietary folate intake and antral follicle count (AFC) among women seeing treatment for infertility.DesignCohort study.SettingAcademic fertility center.PatientsA total of 552 women attending the Massachusetts General Hospital Fertility Center (2007-2019) who participated in the Environment and Reproductive Health Study.InterventionsNone. Folate intake was measured with a validated food frequency questionnaire at study entry. Multivariable Poisson regression models with robust standard errors were used to estimate the association of folate intake with AFC adjusting for calorie intake, age, body mass index, physical activity, education, smoking status, year of AFC, and intakes of vitamin B12, iron, and vitamin D. Nonlinearity was assessed with restricted cubic splines.Main outcome measureAFC as measured by transvaginal ultrasonography as part of routine care.ResultsAmong the 552 women (median age, 35.0 years; median folate intake, 1,005 μg/d), total and supplemental folate intake had a significant nonlinear relationship with AFC. There was a positive linear association with AFC up to approximately 1,200 μg/d for total folate intake and up to 800 μg/d for supplemental folate intake; however, there was no additional benefit of higher folate intakes. The magnitude of the association was modest; for example, the predicted adjusted difference in AFC between a woman consuming 400 vs. 800 μg/d of supplemental folate was approximately 1.5 follicles.ConclusionHigher intake of folate, particularly from supplements, was associated with modestly higher ovarian reserve as measured by AFC among women attending a fertility center.Clinical trial registration numberThis trial was registered at clinicaltrials.gov as NCT00011713.
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Project description:BackgroundCerebrovascular diseases play an important role in dementia. Air pollution is associated with cardiovascular disease, with growing links to neurodegeneration. Prior studies demonstrate associations between fine particulate matter (PM2.5) and biomarkers of endothelial injury in the blood; however, no studies have evaluated these biomarkers in cerebrospinal fluid (CSF).ObjectiveWe evaluate associations between short-term and long-term PM2.5 exposure with CSF vascular cell adhesion molecule-1 (VCAM-1) and e-selectin in cognitively normal and mild cognitive impairment (MCI)/Alzheimer's disease (AD) individuals.MethodsWe collected CSF from 133 community volunteers at VA Puget Sound between 2001-2012. We assigned short-term PM2.5 from central monitors and long-term PM2.5 based on annual average exposure predictions linked to participant addresses. We performed analyses stratified by cognitive status and adjusted for key covariates with tiered models. Our primary exposure windows for the short-term and long-term analyses were 7-day and 1-year averages, respectively.ResultsAmong cognitively normal individuals, a 5 μg/m3 increase in 7-day and 1-year average PM2.5 was associated with elevated VCAM-1 (7-day: 35.4 (9.7, 61.1) ng/ml; 1-year: 51.8 (6.5, 97.1) ng/ml). A 5 μg/m3 increase in 1-year average PM2.5, but not 7-day average, was associated with elevated e-selectin (53.3 (11.0, 95.5) pg/ml). We found no consistent associations among MCI/AD individuals.ConclusionsWe report associations between short-term and long term PM2.5 and CSF biomarkers of vascular damage in cognitively normal adults. These results are aligned with prior research linking PM2.5 to vascular damage in other biofluids as well as emerging evidence of the role of PM2.5 in neurodegeneration.
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