In the past decade there have been an increasing number of scientific studies describing possible effects of air pollution on perinatal health. These papers have mostly focused on commonly monitored air pollutants, primarily ozone (O(3)), particulate matter (PM), sulfur dioxide (SO(2)), carbon monoxide (CO), and nitrogen dioxide (NO(2)), and various indices of perinatal health, including fetal growth, pregnancy duration, and infant mortality. While most published studies have found some marker of air pollution related to some types of perinatal outcomes, variability exists in the nature of the pollutants and outcomes associated. Synthesis of the findings has been difficult for various reasons, including differences in study design and analysis. A workshop was held in September 2007 to discuss methodological differences in the published studies as a basis for understanding differences in study findings and to identify priorities for future research, including novel approaches for existing data. Four broad topic areas were considered: confounding and effect modification, spatial and temporal exposure variations, vulnerable windows of exposure, and multiple pollutants. Here we present a synopsis of the methodological issues and challenges in each area and make recommendations for future study. Two key recommendations include: (1) parallel analyses of existing data sets using a standardized methodological approach to disentangle true differences in associations from methodological differences among studies; and (2) identification of animal studies to inform important mechanistic research gaps. This work is of critical public health importance because of widespread exposure and because perinatal outcomes are important markers of future child and adult health.
BackgroundA more comprehensive estimate of environmental quality would improve our understanding of the relationship between environmental conditions and human health. An environmental quality index (EQI) for all counties in the U.S. was developed.MethodsThe EQI was developed in four parts: domain identification; data source acquisition; variable construction; and data reduction. Five environmental domains (air, water, land, built and sociodemographic) were recognized. Within each domain, data sources were identified; each was temporally (years 2000–2005) and geographically (county) restricted. Variables were constructed for each domain and assessed for missingness, collinearity, and normality. Domain-specific data reduction was accomplished using principal components analysis (PCA), resulting in domain-specific indices. Domain-specific indices were then combined into an overall EQI using PCA. In each PCA procedure, the first principal component was retained. Both domain-specific indices and overall EQI were stratified by four rural–urban continuum codes (RUCC). Higher values for each index were set to correspond to areas with poorer environmental quality.ResultsConcentrations of included variables differed across rural–urban strata, as did within-domain variable loadings, and domain index loadings for the EQI. In general, higher values of the air and sociodemographic indices were found in the more metropolitan areas and the most thinly populated areas have the lowest values of each of the domain indices. The less-urbanized counties (RUCC 3) demonstrated the greatest heterogeneity and range of EQI scores (−4.76, 3.57) while the thinly populated strata (RUCC 4) contained counties with the most positive scores (EQI score ranges from −5.86, 2.52).ConclusionThe EQI holds promise for improving our characterization of the overall environment for public health. The EQI describes the non-residential ambient county-level conditions to which residents are exposed and domain-specific EQI loadings indicate which of the environmental domains account for the largest portion of the variability in the EQI environment. The EQI was constructed for all counties in the United States, incorporating a variety of data to provide a broad picture of environmental conditions. We undertook a reproducible approach that primarily utilized publically-available data sources.
The data sources identified for use in the EQI may be useful to researchers, advocates, and communities to explore specific environmental quality questions.
The aim of this study was to use computer-assisted sperm analysis (CASA) to examine changes in motion parameters of rat spermatozoa incubated under culture conditions that support IVF. Rat cauda epididymal spermatozoa were evaluated in six replicate experiments, at 0 and 4h of incubation. CASA was conducted at 60 Hz on digital 1s tracks ( approximately 100 spermatozoa/rat). Mean values of CASA parameters that describe the vigour of spermatozoa [curvilinear velocity (VCL), amplitude of lateral head displacement (ALH) and beat cross frequency (BCF)] increased, while those indicating progressiveness [straight line velocity (VSL), linearity (LIN) and straightness (STR)] decreased between 0 and 4 h. Visual inspection of sperm tracks after 4 h of incubation revealed classical hyperactivation patterns. Bivariate models were evaluated to objectively define the subpopulation of hyperactivated (HA) spermatozoa. Of all models considered, ALH and LIN, VCL and LIN, BCF and LIN, VCL and BCF, and VCL and ALH showed significant changes in the percentage of HA spermatozoa after the 4 h incubation period. The efficacy of detecting HA spermatozoa was evaluated using sperm tracks that were visually classified as HA or progressive. VCL and LIN provided the most accurate prediction of HA spermatozoa. It was concluded that analysis of CASA data using bivariate models could be used to detect and monitor hyperactivation in rat spermatozoa.
At the levels observed in our study, arsenic does not appear to contribute to adverse birth outcomes. Exposure may play a role in neonatal death; however, the neonatal death rate in this population was low and this potential association merits further research.
ObjectiveThe purpose of this review is to evaluate the impact of recent epidemiologic literature on the National Research Council (NRC) assessment of the lung and bladder cancer risks from ingesting low concentrations (< 100 μg/L) of arsenic-contaminated water.Data sources, extraction, and synthesisPubMed was searched for epidemiologic studies pertinent to the lung and bladder cancer risk estimates from low-dose arsenic exposure. Articles published from 2001, the date of the NRC assessment, through September 2010 were included. Fourteen epidemiologic studies on lung and bladder cancer risk were identified as potentially useful for the analysis.ConclusionsRecent epidemiologic studies that have investigated the risk of lung and bladder cancer from low arsenic exposure are limited in their ability to detect the NRC estimates of excess risk because of sample size and less than lifetime exposure. Although the ecologic nature of the Taiwanese studies on which the NRC estimates are based present certain limitations, the data from these studies have particular strengths in that they describe lung and bladder cancer risks resulting from lifetime exposure in a large population and remain the best data on which to conduct quantitative risk assessment. Continued follow-up of a population in northeastern Taiwan, however, offers the best opportunity to improve the cancer risk assessment for arsenic in drinking water. Future studies of arsenic < 100 μg/L in drinking water and lung and bladder cancer should consider adequacy of the sample size, the synergistic relationship of arsenic and smoking, duration of arsenic exposure, age when exposure began and ended, and histologic subtype.
Background: Particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) has been variably associated with preterm birth (PTB).Objective: We classified PTB into four categories (20–27, 28–31, 32–34, and 35–36 weeks completed gestation) and estimated risk differences (RDs) for each category in association with a 1-μg/m3 increase in PM2.5 exposure during each week of gestation.Methods: We assembled a cohort of singleton pregnancies that completed ≥ 20 weeks of gestation during 2000–2005 using live birth certificate data from three states (Pennsylvania, Ohio, and New Jersey) (n = 1,940,213; 8% PTB). We estimated mean PM2.5 exposures for each week of gestation from monitor-corrected Community Multi-Scale Air Quality modeling data. RDs were estimated using modified Poisson linear regression and adjusted for maternal race/ethnicity, marital status, education, age, and ozone.Results: RD estimates varied by exposure window and outcome period. Average PM2.5 exposure during the fourth week of gestation was positively associated with all PTB outcomes, although magnitude varied by PTB category [e.g., for a 1-μg/m3 increase, RD = 11.8 (95% CI: –6, 29.2); RD = 46 (95% CI: 23.2, 68.9); RD = 61.1 (95% CI: 22.6, 99.7); and RD = 28.5 (95% CI: –39, 95.7) for preterm births during 20–27, 28–31, 32–34, and 35–36 weeks, respectively]. Exposures during the week of birth and the 2 weeks before birth also were positively associated with all PTB categories.Conclusions: Exposures beginning around the time of implantation and near birth appeared to be more strongly associated with PTB than exposures during other time periods. Because particulate matter exposure is ubiquitous, evidence of effects of PM2.5 exposure on PTB, even if small in magnitude, is cause for concern.Citation: Rappazzo KM, Daniels JL, Messer LC, Poole C, Lobdell DT. 2014. Exposure to fine particulate matter during pregnancy and risk of preterm birth among women in New Jersey, Ohio, and Pennsylvania, 2000–2005. Environ Health Perspect 122:992–997; http://dx.doi.org/10.1289/ehp.1307456
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