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Catherine J Karr - One of the best experts on this subject based on the ideXlab platform.
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a cohort study of traffic related air pollution impacts on birth outcomes
Environmental Health Perspectives, 2008Co-Authors: Michael Brauer, Cornel Lencar, Lillian Tamburic, Mieke Koehoorn, Paul A Demers, Catherine J KarrAbstract:Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure. Previous studies have been reviewed in detail. Sram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of Statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes. Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006). Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California—a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations. The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes—fetal growth restriction and inadequate gestational length—are incompletely understood and imperfectly represented in routinely available perinatal measurements available in Vital Statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992). LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003). The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
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a cohort study of traffic related air pollution impacts on birth outcomes
Environmental Health Perspectives, 2008Co-Authors: Michael Brauer, Cornel Lencar, Lillian Tamburic, Mieke Koehoorn, Paul A Demers, Catherine J KarrAbstract:Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure. Previous studies have been reviewed in detail. Sram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of Statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes. Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006). Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California—a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations. The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes—fetal growth restriction and inadequate gestational length—are incompletely understood and imperfectly represented in routinely available perinatal measurements available in Vital Statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992). LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003). The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
Michael H. Malloy - One of the best experts on this subject based on the ideXlab platform.
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Trends in postneonatal aspiration deaths and reclassification of sudden infant death syndrome: Impact of the back to Sleep program
Pediatrics, 2002Co-Authors: Michael H. MalloyAbstract:Objective. The introduction of the “Back to Sleep” campaign for the prevention of sudden infant death syndrome (SIDS) brought with it concern that there might be an increase in the incidence of aspiration-related deaths. The objective of this analysis was to describe the trends in postneonatal mortality and proportionate mortality ratios for the United States for the years 1991 to 1996 for aspiration-related deaths and other causes to which a SIDS death could conceivably be reclassified. Methods. Linked birth and infant death Vital Statistic files for the United States were used for the years 1991, 1995, and 1996. US Vital Statistic Mortality files for the years 1992, 1993, and 1994 were used because of the absence of linked files for those years. Results. The overall postneonatal mortality rate between 1991 and 1996 declined 21.9%, whereas the SIDS rate declined 38.9%. The proportion of the postneonatal mortality (PNPMR) contributed by SIDS declined from 37.1% in 1991 to 28.8% in 1996. There was no significant increase in the PNPMR for aspiration, asphyxia, or respiratory failure. There was, however, a significant increase in the PNPMR for suffocation in bed or cradle from 0.9 to 1.3. Conclusions. These data show no evidence of an increased risk of death from aspiration as a result of the “Back to Sleep” program. Although there has been an increase in the proportion of postneonatal mortality attributable to suffocation, this represents a very small proportion of postneonatal mortality and thus potentially a very small number of SIDS deaths reclassified as suffocation.
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Respiratory Distress Syndrome Mortality In the United States, 1987 to 1995
Journal of Perinatology, 2000Co-Authors: Michael H. Malloy, Daniel H FreemanAbstract:OBJECTIVE: To review respiratory distress syndrome (RDS) mortality since the introduction of surfactant. DESIGN: Population-based historical cohort study. METHODS: United States Vital Statistic data were used for the years 1987 to 1995. Linked birth and infant death file data were available for the years 1987 to 1991 and for 1995. US natality and mortality files were used for the years 1992 to 1994. RESULTS: Whereas overall infant mortality decreased 25% over the-9 year period from a rate of 979 deaths/100,000 live births (LB) to a rate of 736, mortality attributed to RDS decreased 56% from a rate of 84 to 37. The crude black:white relative risk for RDS-related mortality increased from 2.02 in 1987 to 2.76 in 1995. The largest and most consistent drop in RDS-related mortality occurred in the 2000 to 2499 gm birth weight and 33- to 36-week gestation groups; average annual decline=20%. There was a change in the distribution of the underlying causes of death over the 9-year period with an increase in the proportion of mortality attributed to prematurity. CONCLUSION: Since the advent of surfactant there has been a marked reduction in mortality attributed to RDS. Of concern is the increasing disparity between black and white RDS-related mortality.
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Birth weight- and gestational age-specific sudden infant death syndrome mortality: United States, 1991 versus 1995.
Pediatrics, 2000Co-Authors: Michael H. Malloy, Daniel H FreemanAbstract:OBJECTIVE To estimate the changes in birth weight- and gestational age-specific sudden infant death syndrome (SIDS) mortality rates since the publication of the sleep-positioning recommendations by the American Academy of Pediatrics Task Force on Infant Positioning and SIDS. METHODS This is a historical cohort study using US Vital Statistic linked birth and infant death certificate files for the years 1991 and 1995. SIDS deaths were identified as any death attributed to International Classification of Diseases, Ninth Revision code 7980, occurring between the 28th and 365th days of life. RESULTS There were 4871 deaths attributed to SIDS in 1991 for a postneonatal mortality rate of 1.2/1000 postneonatal survivors compared with 3114 deaths in 1995 for a rate of.8/1000. This represents a 33% drop in the postneonatal SIDS mortality from 1991 to 1995. Between 1991 and 1995, SIDS rates declined 38%, 38%, 35%, and 32% for birth weight groupings of 500 to 999 g, 1000 to 1499 g, 1500 to 2499 g, and >/=2500 g, respectively. There were no SIDS deaths attributed to infants weighing /=37 weeks. The rate of decline did not differ significantly across birth weight- or gestational age-specific categories. There was a significant increase in the black:non-black postneonatal SIDS mortality ratio from 2.00 to 2.28, reflecting a smaller decline in birth weight- and gestational age-specific mortality for blacks than observed for the non-black population. CONCLUSION Postneonatal SIDS mortality decreased significantly across all broad birth weight and gestational age categories. If the decline in the prevalence of prone positioning that has been reported since 1992 has occurred across all birth weight and gestational age, these data support the hypothesis that supine or side sleep positioning is effective in preterm/low birth weight infants as well as term infants.
Michael Brauer - One of the best experts on this subject based on the ideXlab platform.
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a cohort study of traffic related air pollution impacts on birth outcomes
Environmental Health Perspectives, 2008Co-Authors: Michael Brauer, Cornel Lencar, Lillian Tamburic, Mieke Koehoorn, Paul A Demers, Catherine J KarrAbstract:Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure. Previous studies have been reviewed in detail. Sram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of Statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes. Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006). Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California—a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations. The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes—fetal growth restriction and inadequate gestational length—are incompletely understood and imperfectly represented in routinely available perinatal measurements available in Vital Statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992). LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003). The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
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a cohort study of traffic related air pollution impacts on birth outcomes
Environmental Health Perspectives, 2008Co-Authors: Michael Brauer, Cornel Lencar, Lillian Tamburic, Mieke Koehoorn, Paul A Demers, Catherine J KarrAbstract:Numerous studies have indicated associations between exposure to ambient air pollution and adverse pregnancy outcomes. Such associations, if determined to be causal, are likely to result in significant public health impacts given the widespread exposure to air pollution and the fact that low birth weight (LBW) or preterm births are subsequently associated with long-term sequelae such as developmental disability and chronic lung disease (Cano et al. 2001; Dik et al. 2004). Determination of a causal relationship between air pollution and adverse pregnancy outcomes would have implications for burden of disease measures and add to the importance of strategies to mitigate the health effects of air pollution exposure. Previous studies have been reviewed in detail. Sram et al. (2005) concluded that evidence is sufficient to support a causal association between ambient concentrations of particulate matter and LBW, but evidence of effects for other pollutants and for other outcomes such as preterm birth is less robust. Maisonet et al. (2004) concluded that studies to date support small effects of air pollution on preterm birth and small for gestational age birth (SGA), but not full-term LBW. In a systematic review, Glinianaia et al. (2004) suggested that evidence of associations with air pollution and fetal growth or pregnancy duration is limited and inconclusive and argued for population-based cohort designs using high-quality individual exposure estimates. These reviews highlight the difficulties in interpreting an evidence base with differences among methods and with important limitations. First, most studies are either time-series studies (Dugandzic et al. 2006; Liu et al. 2003, 2007; Mannes et al. 2005; Sagiv et al. 2005) that relate relatively short-term changes in air pollution concentrations to temporal changes in rates of adverse pregnancy outcomes or, less frequently, cohort analyses that compare outcomes between locations with differing levels of ambient air pollution (Salam et al. 2005) based on interpolated ambient monitoring network data. Between-city comparisons are subject to potential confounding because covariates may be highly correlated with air pollution, whereas time-series studies are problematic to interpret because they relate short-term changes in air pollution that are driven primarily by meteorology to outcomes. They inherently assume that the impact of air pollution on birth outcomes is acute, require knowledge of the relevant periods of pregnancy during which air pollution may have impacts, and are subject to potential confounding by seasonally varying factors. As reviewed by Glinianaia et al. (2004), a number of studies have suggested stronger relationships between birth outcomes and exposure during specific periods of pregnancy based on comparison of Statistical effect sizes. However, results across studies have not consistently identified specific periods of exposure that are most closely linked to adverse pregnancy outcomes. Increasingly, air pollution researchers have identified important spatial variability in air pollution concentrations within airsheds (Hoek et al. 2002b; Lewne et al. 2004; Zhang et al. 2004; Zhu et al. 2004). In many situations these contrasts are of greater magnitude than between-city or temporal contrasts (Jerrett et al. 2005). Such spatial contrasts, primarily related to measures of proximity to traffic corridors, have been associated with a number of health impacts including mortality (Hoek et al. 2002a; Maynard et al. 2007; Miller et al. 2007; Nafstad et al. 2004; Roemer and van Wijnen 2001), asthma and respiratory symptoms (Bayer-Oglesby et al. 2006; Brauer et al. 2002, 2007; Gauderman et al. 2005, 2007; McConnell et al. 2006; Ryan et al. 2005; Smargiassi et al. 2006), and otitis media (Brauer et al. 2006). Application of within-airshed spatial contrasts in birth outcome studies are few (Leem et al. 2006; Parker et al. 2005; Ritz and Yu 1999; Ritz et al. 2000; Slama et al. 2007; Wilhelm and Ritz 2003, 2005). These studies, though provocative, have been limited largely to Southern California—a metropolitan area with relatively high levels of ambient air pollution. They relied on interpolated ambient monitoring data or simple road proximity measures rather than high-resolution spatial contrasts in concentrations. We sought to assess the relationship between reproductive outcomes and spatial and temporally varying levels of air pollution in the metropolitan area of Vancouver, British Columbia, Canada, a city with relatively low levels of ambient air pollution. We estimated exposures at the individual level, for a population-based cohort using both monitor-based methods and land use regression models based on proximity to traffic sources, land use, population density, and topographic features. Even in Vancouver, an area with a dense ambient monitoring network, exposure assessment based on regulatory monitoring network data is more suited to characterizing temporal variability. Land use regression models, even those with temporal components, as in this analysis, focus on high-resolution spatial variability in air pollutant concentrations. The literature describing associations between air pollution and birth outcomes has focused on clinically defined outcomes of LBW and preterm birth, defined in a variety of ways, which complicates comparisons. The underlying biological processes—fetal growth restriction and inadequate gestational length—are incompletely understood and imperfectly represented in routinely available perinatal measurements available in Vital Statistic records. We elected to focus on SGA births as a primary outcome measure, because birth weight as a function of gestational age has a direct effect on perinatal morbidity and mortality (Pollack and Divon 1992). LBW may result from complex and multiple pathways of fetal growth restriction attributed to maternal, fetal, or placental factors. Three broad categories of biological factors have been suggested to play a role in inadequate fetal gestation: abnormality of the biological clock, abnormal implantation, and infection and inflammation (Mattison et al. 2003). The current theories provide multiple sites at which environmental factors may influence biological factors to modulate fetal growth and induce preterm birth. However, specific toxicologic mechanisms including relevant timing during gestational development are not known. We explored each of these processes, fetal growth restriction and inadequate gestational length, separately, and explored the influences of exposure timing in early and late pregnancy.
Isaac Delke - One of the best experts on this subject based on the ideXlab platform.
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Pregnancy-Related Deaths, Florida, 1999–2012: Opportunities to Improve Maternal Outcomes
Maternal and Child Health Journal, 2018Co-Authors: Leticia E. Hernandez, William M. Sappenfield, Karen Harris, Deborah Burch, Washington C. Hill, Cheryl L. Clark, Isaac DelkeAbstract:Objectives To examine pregnancy-related deaths (PRDs) in Florida, to identify quality improvement (QI) opportunities, and to recommend strategies aimed at reducing maternal mortality. Methods The Florida Pregnancy-Associated Mortality Review (PAMR) Committee reviewed PRDs occurring between 1999 and 2012. The PAMR Committee determined causes of PRDs, identified contributing factors, and generated recommendations for prevention and quality improvement. Information from the PAMR data registry, and live births from Florida Vital Statistic data were used to calculate pregnancy-related mortality ratios (PRMR) and PRD univariate risk ratios (RR) with 95% confidence intervals (CI). Results Between 1999 and 2012, the PRMR fluctuated between 14.7 and 26.2 PRDs per 100,000 live births. The five leading causes of PRD were hypertensive disorders (15.5%), hemorrhage (15.2%), infection (12.7%), cardiomyopathy (11.1%), and thrombotic embolism (10.2%), which accounted for 65% of PRDs. Principal contributing factors were morbid obesity (RR = 7.0, 95% CI 4.9–10.0) and late/no prenatal care (RR = 4.2, 95% CI 3.1–5.6). The PRMR for black women was three-fold higher (RR = 3.3, 95% CI 2.7–4.0) than white women. Among the five leading causes of PRDs, 42.5% had at least one clinical care or health care system QI opportunity. Two-third of these were associated with clinical quality of care, which included standards of care, coordination, collaboration, and communication. The QI opportunities varied by PRD cause, but not by race/ethnicity. Conclusion Gaps in clinical care or health care systems were assessed as the primary factors in over 40% of PRDs leading the PAMR Committee to generate QI recommendations for clinical care and health care systems.
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Pregnancy-Related Deaths, Florida, 1999-2012: Opportunities to Improve Maternal Outcomes.
Maternal and child health journal, 2017Co-Authors: Leticia E. Hernandez, William M. Sappenfield, Deborah Burch, Washington C. Hill, Cheryl L. Clark, Karen E. Harris, Isaac DelkeAbstract:Objectives To examine pregnancy-related deaths (PRDs) in Florida, to identify quality improvement (QI) opportunities, and to recommend strategies aimed at reducing maternal mortality. Methods The Florida Pregnancy-Associated Mortality Review (PAMR) Committee reviewed PRDs occurring between 1999 and 2012. The PAMR Committee determined causes of PRDs, identified contributing factors, and generated recommendations for prevention and quality improvement. Information from the PAMR data registry, and live births from Florida Vital Statistic data were used to calculate pregnancy-related mortality ratios (PRMR) and PRD univariate risk ratios (RR) with 95% confidence intervals (CI). Results Between 1999 and 2012, the PRMR fluctuated between 14.7 and 26.2 PRDs per 100,000 live births. The five leading causes of PRD were hypertensive disorders (15.5%), hemorrhage (15.2%), infection (12.7%), cardiomyopathy (11.1%), and thrombotic embolism (10.2%), which accounted for 65% of PRDs. Principal contributing factors were morbid obesity (RR = 7.0, 95% CI 4.9–10.0) and late/no prenatal care (RR = 4.2, 95% CI 3.1–5.6). The PRMR for black women was three-fold higher (RR = 3.3, 95% CI 2.7–4.0) than white women. Among the five leading causes of PRDs, 42.5% had at least one clinical care or health care system QI opportunity. Two-third of these were associated with clinical quality of care, which included standards of care, coordination, collaboration, and communication. The QI opportunities varied by PRD cause, but not by race/ethnicity. Conclusion Gaps in clinical care or health care systems were assessed as the primary factors in over 40% of PRDs leading the PAMR Committee to generate QI recommendations for clinical care and health care systems.
Daniel H Freeman - One of the best experts on this subject based on the ideXlab platform.
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Respiratory Distress Syndrome Mortality In the United States, 1987 to 1995
Journal of Perinatology, 2000Co-Authors: Michael H. Malloy, Daniel H FreemanAbstract:OBJECTIVE: To review respiratory distress syndrome (RDS) mortality since the introduction of surfactant. DESIGN: Population-based historical cohort study. METHODS: United States Vital Statistic data were used for the years 1987 to 1995. Linked birth and infant death file data were available for the years 1987 to 1991 and for 1995. US natality and mortality files were used for the years 1992 to 1994. RESULTS: Whereas overall infant mortality decreased 25% over the-9 year period from a rate of 979 deaths/100,000 live births (LB) to a rate of 736, mortality attributed to RDS decreased 56% from a rate of 84 to 37. The crude black:white relative risk for RDS-related mortality increased from 2.02 in 1987 to 2.76 in 1995. The largest and most consistent drop in RDS-related mortality occurred in the 2000 to 2499 gm birth weight and 33- to 36-week gestation groups; average annual decline=20%. There was a change in the distribution of the underlying causes of death over the 9-year period with an increase in the proportion of mortality attributed to prematurity. CONCLUSION: Since the advent of surfactant there has been a marked reduction in mortality attributed to RDS. Of concern is the increasing disparity between black and white RDS-related mortality.
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Birth weight- and gestational age-specific sudden infant death syndrome mortality: United States, 1991 versus 1995.
Pediatrics, 2000Co-Authors: Michael H. Malloy, Daniel H FreemanAbstract:OBJECTIVE To estimate the changes in birth weight- and gestational age-specific sudden infant death syndrome (SIDS) mortality rates since the publication of the sleep-positioning recommendations by the American Academy of Pediatrics Task Force on Infant Positioning and SIDS. METHODS This is a historical cohort study using US Vital Statistic linked birth and infant death certificate files for the years 1991 and 1995. SIDS deaths were identified as any death attributed to International Classification of Diseases, Ninth Revision code 7980, occurring between the 28th and 365th days of life. RESULTS There were 4871 deaths attributed to SIDS in 1991 for a postneonatal mortality rate of 1.2/1000 postneonatal survivors compared with 3114 deaths in 1995 for a rate of.8/1000. This represents a 33% drop in the postneonatal SIDS mortality from 1991 to 1995. Between 1991 and 1995, SIDS rates declined 38%, 38%, 35%, and 32% for birth weight groupings of 500 to 999 g, 1000 to 1499 g, 1500 to 2499 g, and >/=2500 g, respectively. There were no SIDS deaths attributed to infants weighing /=37 weeks. The rate of decline did not differ significantly across birth weight- or gestational age-specific categories. There was a significant increase in the black:non-black postneonatal SIDS mortality ratio from 2.00 to 2.28, reflecting a smaller decline in birth weight- and gestational age-specific mortality for blacks than observed for the non-black population. CONCLUSION Postneonatal SIDS mortality decreased significantly across all broad birth weight and gestational age categories. If the decline in the prevalence of prone positioning that has been reported since 1992 has occurred across all birth weight and gestational age, these data support the hypothesis that supine or side sleep positioning is effective in preterm/low birth weight infants as well as term infants.