Adult air pollution exposure and risk of infertility in the Nurses' Health Study II.
Ontology highlight
ABSTRACT:
SUBMITTER: Mahalingaiah S
PROVIDER: S-EPMC4755443 | biostudies-literature | 2016 Mar
REPOSITORIES: biostudies-literature
Publications
Adult air pollution exposure and risk of infertility in the Nurses' Health Study II.
Mahalingaiah S S Hart J E JE Laden F F Farland L V LV Hewlett M M MM Chavarro J J Aschengrau A A Missmer S A SA
Human reproduction (Oxford, England) 20160102 3
<h4>Study question</h4>Is there an association between air pollution exposures and incident infertility?<h4>Summary answer</h4>Increased exposure to air pollution is associated with an increased incidence of infertility.<h4>What is known already</h4>Exposures to air pollution have been associated with lower conception and fertility rates. However, the impact of pollution on infertility incidence is unknown.<h4>Study design, size, duration</h4>Prospective cohort study using data collected from 11 ...[more]
Similar Datasets
Project description:Study questionIs there an association between air pollution exposures and the risk of spontaneous abortion (SAB)?Summary answerHigher exposure to particulate matter (PM) air pollution above and beyond a woman's average exposure may be associated with greater risk of SAB, particularly among women experiencing at least one SAB during follow-up.What is known alreadyThere is sufficient biologic plausibility to suggest that air pollution adversely affects early pregnancy outcomes, particularly pregnancy loss; however, the evidence is limited.Study design, size, durationOur prospective cohort study included 19 309 women in the Nurses' Health Study II who contributed a total of 35 025 pregnancies between 1990 and 2008. We also conducted a case-crossover analysis among 3585 women (11 212 pregnancies) with at least one SAB and one live birth during follow-up.Participants/materials, setting, methodsProximity to major roadways and exposure to PM <10 microns (PM10), 2.5-10 microns (PM2.5-10) and <2.5 microns (PM2.5) were determined for residential addresses between 1989 and 2007. Pregnancy outcomes were self-reported biannually throughout follow-up and comprehensively in 2009. Multivariable log-binomial regression models with generalized estimating equations were used to estimate the risk ratios and 95% CIs of SAB. Conditional logistic regression was used for the case-crossover analysis.Main results and the role of chanceDuring the 19 years of follow-up, 6599 SABs (18.8% of pregnancies) were reported. In the main analysis, living closer to a major roadway and average exposure to PM10, PM10-2.5 or PM2.5 in the 1 or 2 years prior to pregnancy were not associated with an increased risk of SAB. However, small positive associations between PM exposures and SAB were observed when restricting the analysis to women experiencing at least one SAB during follow-up. In the case-crossover analysis, an increase in PM10 (per 3.9 μg/m3), PM2.5-10 (per 2.3 μg/m3) and PM2.5 (per 2.0 μg/m3) in the year prior to pregnancy was associated with 1.12 (95% CI 1.06, 1.19), 1.09 (95% CI 1.03, 1.14) and 1.10 (95% CI 1.04, 1.17) higher odds of SAB, respectively.Limitations, reasons for cautionWe did not have information on the month or day of SAB, which precluded our ability to examine specific windows of susceptibility or acute exposures. We also used ambient air pollution exposures as a proxy for personal exposure, potentially leading to exposure misclassification.Wider implications of the findingsIn our case-crossover analysis (but not in the entire cohort) we observed positive associations between exposure to all size fractions of PM exposure and risk of SAB. This may suggest that changes in PM exposure confer greater risk of SAB or that women with a history of SAB are a particularly vulnerable subgroup.Study funding/competing interest(s)The authors are supported by the following NIH grants UM1CA176726, R00ES026648 and P30ES000002. The authors have no actual or potential competing financial interests to disclose.
| S-EPMC6736292 | biostudies-literature
Project description:BackgroundFindings from a recent prospective cohort study in California suggested increased risk of breast cancer associated with higher exposure to certain carcinogenic and estrogen-disrupting hazardous air pollutants (HAPs). However, to date, no nationwide studies have evaluated these possible associations. Our objective was to examine the impacts of mammary carcinogen and estrogen disrupting HAPs on risk of invasive breast cancer in a nationwide cohort.MethodsWe assigned HAPs from the US Environmental Protection Agency's 2002 National Air Toxics Assessment to 109,239 members of the nationwide, prospective Nurses' Health Study II (NHSII). Risk of overall invasive, estrogen receptor (ER)-positive (ER+), and ER-negative (ER-) breast cancer with increasing quartiles of exposure were assessed in time-varying multivariable proportional hazards models, adjusted for traditional breast cancer risk factors.ResultsA total of 3321 invasive cases occurred (2160 ER+, 558 ER-) during follow-up 1989-2011. Overall, there was no consistent pattern of elevated risk of the HAPs with risk of breast cancer. Suggestive elevations were only seen with increasing 1,2-dibromo-3-chloropropane exposures (multivariable adjusted HR of overall breast cancer = 1.12, 95% CI: 0.98-1.29; ER+ breast cancer HR = 1.09; 95% CI: 0.92, 1.30; ER- breast cancer HR = 1.14; 95% CI: 0.81, 1.61; each in the top exposure quartile compared to the lowest).ConclusionsExposures to HAPs during adulthood were not consistently associated with an increased risk of overall or estrogen-receptor subtypes of invasive breast cancer in this nationwide cohort of women.
| S-EPMC5870204 | biostudies-literature
Project description:BackgroundA body of literature has suggested an elevated risk of lung cancer associated with particulate matter and traffic-related pollutants.ObjectiveWe examined the relation of lung cancer incidence with long-term residential exposures to ambient particulate matter and residential distance to roadway, as a proxy for traffic-related exposures.MethodsFor participants in the Nurses' Health Study, a nationwide prospective cohort of women, we estimated 72-month average exposures to PM2.5, PM2.5-10, and PM10 and residential distance to road. Follow-up for incident cases of lung cancer occurred from 1994 through 2010. Cox proportional hazards models were adjusted for potential confounders. Effect modification by smoking status was examined.ResultsDuring 1,510,027 person-years, 2,155 incident cases of lung cancer were observed among 103,650 participants. In fully adjusted models, a 10-?g/m3 increase in 72-month average PM10 [hazard ratio (HR) = 1.04; 95% CI: 0.95, 1.14], PM2.5 (HR = 1.06; 95% CI: 0.91, 1.25), or PM2.5-10 (HR = 1.05; 95% CI: 0.92, 1.20) was positively associated with lung cancer. When the cohort was restricted to never-smokers and to former smokers who had quit at least 10 years before, the associations appeared to increase and were strongest for PM2.5 (PM10: HR = 1.15; 95% CI: 1.00, 1.32; PM2.5: HR = 1.37; 95% CI: 1.06, 1.77; PM2.5-10: HR = 1.11; 95% CI: 0.90, 1.37). RESULTS were most elevated when restricted to the most prevalent subtype, adenocarcinomas. Risks with roadway proximity were less consistent.ConclusionsOur findings support those from other studies indicating increased risk of incident lung cancer associated with ambient PM exposures, especially among never- and long-term former smokers.
| S-EPMC4154215 | biostudies-literature
Project description:The study comprises of 24 subjects that have been exposed to high and low Traffic-related air pollution.
2022-01-01 | GSE125647 | GEO
Project description:Background:Ultraviolet (UV) radiation exposure, the primary source of vitamin D for most people, may reduce breast cancer risk. To date, epidemiologic studies have shown inconsistent results. Methods:The Nurses' Health Study II is a U.S. nationwide prospective cohort of female registered nurses. A UV exposure model was linked with geocoded residential address histories. Early-life UV exposure was estimated based on the state of residence at birth, age 15, and age 30. Self-reported breast cancer was confirmed from medical records. Time-varying Cox regression models adjusted for established breast cancer risk factors were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). Results:From 1989 to 2013, 3,959 invasive breast cancer cases occurred among 112,447 participants. Higher UV exposure during adulthood was not associated with invasive breast cancer risk overall (adjusted HR comparing highest to lowest quintile = 1.00, 95% CI: 0.90, 1.11, p for trend = 0.64) or according to estrogen receptor (ER) status. There were suggestive inverse associations between ER- breast cancer and early-life UV exposure at birth (adjusted HR = 0.94, 95% CI: 0.88, 1.01 per interquartile range increase [15.7 mW/m2]), age 15 (adjusted HR = 0.96, 95% CI: 0.89, 1.04 per 18.0 mW/m2), and age 30 (adjusted HR = 0.90, 95% CI: 0.82, 1.00 per 27.7 mW/m2). Conclusions:Ambient UV exposure during adulthood was not associated with risk of invasive breast cancer overall or by ER status. However, we observed suggestive inverse associations between early-life UV exposure and ER- breast cancer risk.
| S-EPMC6639017 | biostudies-literature
Project description:The Global Burden of Disease assessment estimates that 20% of global type 2 diabetes cases are related to chronic exposure to particulate matter (PM) with a diameter of 2·5 μm or less (PM2·5). With 99% of the global population residing in areas where air pollution levels are above current WHO air quality guidelines, and increasing concern in regard to the common drivers of air pollution and climate change, there is a compelling need to understand the connection between air pollution and cardiometabolic disease, and pathways to address this preventable risk factor. This Review provides an up to date summary of the epidemiological evidence and mechanistic underpinnings linking air pollution with cardiometabolic risk. We also outline approaches to improve awareness, and discuss personal-level, community, governmental, and policy interventions to help mitigate the growing global public health risk of air pollution exposure.
| S-EPMC11264310 | biostudies-literature
Project description:BackgroundEnvironmental factors have been identified as primary risk factors for type 2 diabetes mellitus (T2DM). However, studies on the association between environmental factors and T2DM have mainly focused on morbidity and mortality, which do not fully reflect the disease burden stemming from air pollution. Therefore, we aimed to evaluate the correlation between air pollution and T2DM, including hospital length of stay (LOS) and costs.MethodsWe collected data on patients with T2DM from three healthcare institutions in Xinxiang from 2016-2021. Data on particulate and gaseous pollutants in Xinxiang and daily meteorological data were collected from national databases. The distribution lag nonlinear model was used to evaluate the correlation between air pollution and the number of inpatients with T2DM, LOS, and hospital costs. Subgroup analyses were conducted to identify potential modifying factors.ResultsOverall, 13,797 patients with T2DM were included in our analysis. Within the cumulative lag of 7 days, with every increase of 1 mg/m3 of carbon monoxide (CO) and 10 μg/m3 of 2.5 microns particulate matter, nitrogen dioxide and ozone exhibited significant associations with an increase in diabetes hospitalization risk. CO exhibited adverse effects on LOS on most lag days. Moreover, hospital costs were significantly associated with the attributable fraction of LOS and hospital costs attributed to diabetes.ConclusionsExposure to air pollutants increased T2DM risk, imposing significant economic and social burdens in Xinxiang, China. Implementing policies to reduce air pollutant exposure may decrease T2DM admissions, costs, and LOS.
| S-EPMC11653192 | biostudies-literature
Project description:Depression is a leading mental health disorder worldwide, contributing substantially to the global disease burden. While emerging evidence suggests links between specific air pollutants and depression, the potential interactions among multiple pollutants remain underexplored. Here we show the influence of six common air pollutants on depressive symptoms among middle-aged and older Chinese adults. In single-pollutant models, a 10 μg m-3 increase in SO2, CO, PM10, and PM2.5 is associated with increased risks of depressive symptoms, with odds ratios (95% confidence intervals) of 1.276 (1.238-1.315), 1.007 (1.006-1.008), 1.066 (1.055-1.078), and 1.130 (1.108-1.153), respectively. In two-pollutant models, SO2 remains significantly associated with depressive symptoms after adjusting for other pollutants. Multi-pollutant models uncover synergistic effects, with SO2, CO, NO2, PM10, and PM2.5 exhibiting significant interactions, identifying SO2 as the primary driver of these associations. Mediation analyses further indicate that cognitive and physical impairments partially mediate the relationship between air pollution and depressive symptoms. These findings underscore the critical mental health impacts of air pollution and highlight the need for integrated air quality management strategies. Targeted mitigation of specific pollutants, particularly SO2, is expected to significantly enhance public mental health outcomes.
| S-EPMC11647501 | biostudies-literature
Project description:The proportional hazards (PH) model is commonly used in epidemiology despite the stringent assumption of proportionality of hazards over time. We previously showed, using detailed simulation data, that the impact of a modest risk factor cannot be estimated reliably using the PH model in the presence of confounding by a strong, time-dependent risk factor. Here, we examine the same and related issues using a real dataset. Among 97,303 women in the prospective Nurses' Health Study cohort from 1994 through 2010, we used PH regression to investigate how effect estimates for cigarette smoking are affected by increasingly detailed specification of time-dependent exposure characteristics. We also examined how effect estimates for fine particulate matter (PM2.5), a modest risk factor, are affected by finer control for time-dependent confounding by smoking. The objective of this analysis is not to present a credible estimate of the impact of PM2.5 on lung cancer risk, but to show that estimates based on the PH model are inherently unreliable. The best-fitting model for cigarette smoking and lung cancer included pack-years, duration, time since cessation, and an age-by-pack-years interaction, indicating that the hazard ratio (HR) for pack-years was significantly modified by age. In the fully adjusted best-fitting model for smoking including pack-years, the HR per 10-µg/m3 increase in PM2.5 was 1.06 (95% confidence interval (CI) = 0.90, 1.25); the HR for PM2.5 in the full cohort ranged between 1.02 and 1.10 in models with other smoking adjustments, indicating a residual confounding effect of smoking. The HR for PM2.5 was statistically significant only among former smokers when adjusting for smoking pack-years (HR = 1.35, 95% CI = 1.00, 1.82 in the best-fitting smoking model), but not in models adjusting for smoking duration and average packs (pack-years divided by duration). The association between cumulative smoking and lung cancer is modified by age, and improved model fit is obtained by including multiple time-varying components of smoking history. The association with PM2.5 is residually confounded by smoking and modified by smoking status. These findings underscore limitations of the PH model and emphasize the advantages of directly estimating hazard functions to characterize time-varying exposure and risk. The hazard function, not the relative hazard, is the fundamental measure of risk in a population. As a consequence, the use of time-dependent PH models does not address crucial issues introduced by temporal factors in epidemiological data.
| S-EPMC7269844 | biostudies-literature
Project description:BackgroundAir pollution exposure is associated with cardiovascular morbidity and mortality. Although exposure to air pollution early in life may represent a critical window for development of cardiovascular disease risk factors, few studies have examined associations of long-term air pollution exposure with markers of cardiovascular and metabolic health in young adults.ObjectivesBy combining health data from the National Longitudinal Study of Adolescent to Adult Health (Add Health) with air pollution data from the Fused Air Quality Surface using Downscaling (FAQSD) archive, we: (1) calculated multi-year estimates of exposure to ozone (O3) and particulate matter with an aerodynamic diameter ≤ 2.5 µm (PM2.5) for Add Health participants; and (2) estimated associations between air pollution exposures and multiple markers of cardiometabolic health.MethodsAdd Health is a nationally representative longitudinal cohort study of over 20,000 adolescents aged 12-19 in the United States (US) in 1994-95 (Wave I). Participants have been followed through adolescence and into adulthood with five in-home interviews. Estimated daily concentrations of O3 and PM2.5 at census tracts were obtained from the FAQSD archive and used to generate tract-level annual averages of O3 and PM2.5 concentrations. We estimated associations between average O3 and PM2.5 exposures from 2002 to 2007 and markers of cardiometabolic health measured at Wave IV (2008-09), including hypertension, hyperlipidemia, body mass index (BMI), diabetes, C-reactive protein, and metabolic syndrome.ResultsThe final sample size was 11,259 individual participants. The average age of participants at Wave IV was 28.4 years (range: 24-34 years). In models adjusting for age, race/ethnicity, and sex, long-term O3 exposure (2002-07) was associated with elevated odds of hypertension, with an odds ratio (OR) of 1.015 (95% confidence interval [CI]: 1.011, 1.029); obesity (1.022 [1.004, 1.040]); diabetes (1.032 [1.009,1.054]); and metabolic syndrome (1.028 [1.014, 1.041]); PM2.5 exposure (2002-07) was associated with elevated odds of hypertension (1.022 [1.001, 1.045]).ConclusionFindings suggest that long-term ambient air pollution exposure, particularly O3 exposure, is associated with cardiometabolic health in early adulthood.
| S-EPMC10664021 | biostudies-literature