The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

Beate Ritz - One of the best experts on this subject based on the ideXlab platform.

  • prenatal exposure to Air Toxics and malignant germ cell tumors in young children
    Journal of Occupational and Environmental Medicine, 2019
    Co-Authors: Clinton Hall, Julia E Heck, Beate Ritz, Myles Cockburn, Loraine A Escobedo, Ondine S Von Ehrenstein
    Abstract:

    Author(s): Hall, Clinton; Heck, Julia E; Ritz, Beate; Cockburn, Myles; Escobedo, Loraine A; von Ehrenstein, Ondine S | Abstract: ObjectiveTo assess prenatal Air Toxics exposure and risk for childhood germ cell tumors (GCTs) by histological subtype (yolk sac tumor and teratoma).MethodsIn this case-control study, GCT cases less than 6 years (n = 243) identified from California Cancer Registry records were matched by birth year to cancer-free population controls (n = 147,100), 1984 to 2013. Routinely monitored Air toxic exposures were linked to subjects' birth address. Logistic regression estimated GCT risks per interquartile range increase in exposure.ResultsPrenatal exposure to various highly-correlated, traffic-related Air Toxics during the second trimester increased GCT risk, particularly 1,3-butadiene (odds ratio [OR] = 1.51; 95% confidence interval [CI] = 1.01, 2.26) and meta/para-xylene (OR = 1.56; 95% CI = 1.10, 2.21). Analyses by subtype indicated elevated ORs for yolk sac tumors but not teratomas.ConclusionOur estimated ORs are consistent with positive associations between some prenatal traffic-related Air Toxics and GCT risk, notably yolk sac tumors.

  • retinoblastoma and ambient exposure to Air Toxics in the perinatal period
    Journal of Exposure Science and Environmental Epidemiology, 2015
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    We examined ambient exposure to specific Air Toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 Air Toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an Air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to Air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in Air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other Toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six Toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.

  • risk of leukemia in relation to exposure to ambient Air Toxics in pregnancy and early childhood
    International Journal of Hygiene and Environmental Health, 2014
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to Toxics in ambient Air. In our case-control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children Air Toxics monitoring station between 1990 and 2007. Information on Air Toxics exposures was taken from community Air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in Air toxic exposure. Risk of ALL was elevated with 3(rd) trimester exposure to polycyclic aromatic hydrocarbons (OR=1.16, 95% CI 1.04, 1.29), arsenic (OR=1.33, 95% CI 1.02, 1.73), benzene (OR=1.50, 95% CI 1.08, 2.09), and three other Toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR=1.30, 95% CI 1.00, 1.69), benzene (1.75, 95% CI 1.04, 2.93), and two other traffic-related Toxics. During the child's first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.

  • an exploratory study of ambient Air Toxics exposure in pregnancy and the risk of neuroblastoma in offspring
    Environmental Research, 2013
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    Little is known about the etiology of neuroblastoma, the most common cancer in infancy. In this study, we examined maternal exposure to ambient Air Toxics in pregnancy in relation to neuroblastoma in the child. We ascertained all cases of neuroblastoma listed in the California Cancer Registry 1990-2007 that could be linked to a California birth certificate, and controls were selected at random from California birth records. Average Air Toxics exposures during pregnancy were determined based upon measures from community-based Air pollution monitors. The study included 75 cases and 14,602 controls who lived with 5 km of an Air pollution monitor, and we additionally examined results for those living within a smaller radius around the monitor (2.5 km). Logistic regression was used to determine the risk of neuroblastoma with one interquartile range increase in Air toxic exposure. Neuroblastoma risk was increased with higher maternal exposure to carbon tetrachloride (OR=2.65, 95%CI 1.07, 6.53) and polycyclic aromatic hydrocarbons (OR=1.39, 95%CI 1.05, 1.84), particularly indeno(1,2,3-cd)pyrene and dibenz(a,h)anthracene. Hexavalent chromium was associated with neuroblastoma at the 5 km distance (OR=1.32, 95%CI 1.00, 1.74) but not at the 2.5 km distance. This is one of the first studies to report associations between neuroblastoma and these Air Toxics.

  • assessing the influence of traffic related Air pollution on risk of term low birth weight on the basis of land use based regression models and measures of Air Toxics
    American Journal of Epidemiology, 2012
    Co-Authors: Jo Kay Ghosh, Myles Cockburn, Michelle Wilhelm, Michael Jerrett, Daniel W Goldberg, Beate Ritz
    Abstract:

    Few studies have examined associations of birth outcomes with toxic Air pollutants (Air Toxics) in traffic exhaust. This study included 8,181 term low birth weight (LBW) children and 370,922 term normal-weight children born between January 1, 1995, and December 31, 2006, to women residing within 5 miles (8 km) of an Air Toxics monitoring station in Los Angeles County, California. Additionally, land-use-based regression (LUR)-modeled estimates of levels of nitric oxide, nitrogen dioxide, and nitrogen oxides were used to assess the influence of small-area variations in traffic pollution. The authors examined associations with term LBW (≥37 weeks’ completed gestation and birth weight <2,500 g) using logistic regression adjusted for maternal age, race/ethnicity, education, parity, infant gestational age, and gestational age squared. Odds of term LBW increased 2%–5% (95% confidence intervals ranged from 1.00 to 1.09) per interquartile-range increase in LUR-modeled estimates and monitoring-based Air Toxics exposure estimates in the entire pregnancy, the third trimester, and the last month of pregnancy. Models stratified by monitoring station (to investigate Air Toxics associations based solely on temporal variations) resulted in 2%–5% increased odds per interquartile-range increase in third-trimester benzene, toluene, ethyl benzene, and xylene exposures, with some confidence intervals containing the null value. This analysis highlights the importance of both spatial and temporal contributions to Air pollution in epidemiologic birth outcome studies.

Myles Cockburn - One of the best experts on this subject based on the ideXlab platform.

  • prenatal exposure to Air Toxics and malignant germ cell tumors in young children
    Journal of Occupational and Environmental Medicine, 2019
    Co-Authors: Clinton Hall, Julia E Heck, Beate Ritz, Myles Cockburn, Loraine A Escobedo, Ondine S Von Ehrenstein
    Abstract:

    Author(s): Hall, Clinton; Heck, Julia E; Ritz, Beate; Cockburn, Myles; Escobedo, Loraine A; von Ehrenstein, Ondine S | Abstract: ObjectiveTo assess prenatal Air Toxics exposure and risk for childhood germ cell tumors (GCTs) by histological subtype (yolk sac tumor and teratoma).MethodsIn this case-control study, GCT cases less than 6 years (n = 243) identified from California Cancer Registry records were matched by birth year to cancer-free population controls (n = 147,100), 1984 to 2013. Routinely monitored Air toxic exposures were linked to subjects' birth address. Logistic regression estimated GCT risks per interquartile range increase in exposure.ResultsPrenatal exposure to various highly-correlated, traffic-related Air Toxics during the second trimester increased GCT risk, particularly 1,3-butadiene (odds ratio [OR] = 1.51; 95% confidence interval [CI] = 1.01, 2.26) and meta/para-xylene (OR = 1.56; 95% CI = 1.10, 2.21). Analyses by subtype indicated elevated ORs for yolk sac tumors but not teratomas.ConclusionOur estimated ORs are consistent with positive associations between some prenatal traffic-related Air Toxics and GCT risk, notably yolk sac tumors.

  • retinoblastoma and ambient exposure to Air Toxics in the perinatal period
    Journal of Exposure Science and Environmental Epidemiology, 2015
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    We examined ambient exposure to specific Air Toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 Air Toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an Air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to Air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in Air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other Toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six Toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.

  • risk of leukemia in relation to exposure to ambient Air Toxics in pregnancy and early childhood
    International Journal of Hygiene and Environmental Health, 2014
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to Toxics in ambient Air. In our case-control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children Air Toxics monitoring station between 1990 and 2007. Information on Air Toxics exposures was taken from community Air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in Air toxic exposure. Risk of ALL was elevated with 3(rd) trimester exposure to polycyclic aromatic hydrocarbons (OR=1.16, 95% CI 1.04, 1.29), arsenic (OR=1.33, 95% CI 1.02, 1.73), benzene (OR=1.50, 95% CI 1.08, 2.09), and three other Toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR=1.30, 95% CI 1.00, 1.69), benzene (1.75, 95% CI 1.04, 2.93), and two other traffic-related Toxics. During the child's first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.

  • an exploratory study of ambient Air Toxics exposure in pregnancy and the risk of neuroblastoma in offspring
    Environmental Research, 2013
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    Little is known about the etiology of neuroblastoma, the most common cancer in infancy. In this study, we examined maternal exposure to ambient Air Toxics in pregnancy in relation to neuroblastoma in the child. We ascertained all cases of neuroblastoma listed in the California Cancer Registry 1990-2007 that could be linked to a California birth certificate, and controls were selected at random from California birth records. Average Air Toxics exposures during pregnancy were determined based upon measures from community-based Air pollution monitors. The study included 75 cases and 14,602 controls who lived with 5 km of an Air pollution monitor, and we additionally examined results for those living within a smaller radius around the monitor (2.5 km). Logistic regression was used to determine the risk of neuroblastoma with one interquartile range increase in Air toxic exposure. Neuroblastoma risk was increased with higher maternal exposure to carbon tetrachloride (OR=2.65, 95%CI 1.07, 6.53) and polycyclic aromatic hydrocarbons (OR=1.39, 95%CI 1.05, 1.84), particularly indeno(1,2,3-cd)pyrene and dibenz(a,h)anthracene. Hexavalent chromium was associated with neuroblastoma at the 5 km distance (OR=1.32, 95%CI 1.00, 1.74) but not at the 2.5 km distance. This is one of the first studies to report associations between neuroblastoma and these Air Toxics.

  • assessing the influence of traffic related Air pollution on risk of term low birth weight on the basis of land use based regression models and measures of Air Toxics
    American Journal of Epidemiology, 2012
    Co-Authors: Jo Kay Ghosh, Myles Cockburn, Michelle Wilhelm, Michael Jerrett, Daniel W Goldberg, Beate Ritz
    Abstract:

    Few studies have examined associations of birth outcomes with toxic Air pollutants (Air Toxics) in traffic exhaust. This study included 8,181 term low birth weight (LBW) children and 370,922 term normal-weight children born between January 1, 1995, and December 31, 2006, to women residing within 5 miles (8 km) of an Air Toxics monitoring station in Los Angeles County, California. Additionally, land-use-based regression (LUR)-modeled estimates of levels of nitric oxide, nitrogen dioxide, and nitrogen oxides were used to assess the influence of small-area variations in traffic pollution. The authors examined associations with term LBW (≥37 weeks’ completed gestation and birth weight <2,500 g) using logistic regression adjusted for maternal age, race/ethnicity, education, parity, infant gestational age, and gestational age squared. Odds of term LBW increased 2%–5% (95% confidence intervals ranged from 1.00 to 1.09) per interquartile-range increase in LUR-modeled estimates and monitoring-based Air Toxics exposure estimates in the entire pregnancy, the third trimester, and the last month of pregnancy. Models stratified by monitoring station (to investigate Air Toxics associations based solely on temporal variations) resulted in 2%–5% increased odds per interquartile-range increase in third-trimester benzene, toluene, ethyl benzene, and xylene exposures, with some confidence intervals containing the null value. This analysis highlights the importance of both spatial and temporal contributions to Air pollution in epidemiologic birth outcome studies.

Julia E Heck - One of the best experts on this subject based on the ideXlab platform.

  • prenatal exposure to Air Toxics and malignant germ cell tumors in young children
    Journal of Occupational and Environmental Medicine, 2019
    Co-Authors: Clinton Hall, Julia E Heck, Beate Ritz, Myles Cockburn, Loraine A Escobedo, Ondine S Von Ehrenstein
    Abstract:

    Author(s): Hall, Clinton; Heck, Julia E; Ritz, Beate; Cockburn, Myles; Escobedo, Loraine A; von Ehrenstein, Ondine S | Abstract: ObjectiveTo assess prenatal Air Toxics exposure and risk for childhood germ cell tumors (GCTs) by histological subtype (yolk sac tumor and teratoma).MethodsIn this case-control study, GCT cases less than 6 years (n = 243) identified from California Cancer Registry records were matched by birth year to cancer-free population controls (n = 147,100), 1984 to 2013. Routinely monitored Air toxic exposures were linked to subjects' birth address. Logistic regression estimated GCT risks per interquartile range increase in exposure.ResultsPrenatal exposure to various highly-correlated, traffic-related Air Toxics during the second trimester increased GCT risk, particularly 1,3-butadiene (odds ratio [OR] = 1.51; 95% confidence interval [CI] = 1.01, 2.26) and meta/para-xylene (OR = 1.56; 95% CI = 1.10, 2.21). Analyses by subtype indicated elevated ORs for yolk sac tumors but not teratomas.ConclusionOur estimated ORs are consistent with positive associations between some prenatal traffic-related Air Toxics and GCT risk, notably yolk sac tumors.

  • retinoblastoma and ambient exposure to Air Toxics in the perinatal period
    Journal of Exposure Science and Environmental Epidemiology, 2015
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    We examined ambient exposure to specific Air Toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 Air Toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an Air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to Air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in Air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other Toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six Toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.

  • risk of leukemia in relation to exposure to ambient Air Toxics in pregnancy and early childhood
    International Journal of Hygiene and Environmental Health, 2014
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    There are few established causes of leukemia, the most common type of cancer in children. Studies in adults suggest a role for specific environmental agents, but little is known about any effect from exposures in pregnancy to Toxics in ambient Air. In our case-control study, we ascertained 69 cases of acute lymphoblastic leukemia (ALL) and 46 cases of acute myeloid leukemia (AML) from California Cancer Registry records of children Air Toxics monitoring station between 1990 and 2007. Information on Air Toxics exposures was taken from community Air monitors. We used logistic regression to estimate the risk of leukemia associated with one interquartile range increase in Air toxic exposure. Risk of ALL was elevated with 3(rd) trimester exposure to polycyclic aromatic hydrocarbons (OR=1.16, 95% CI 1.04, 1.29), arsenic (OR=1.33, 95% CI 1.02, 1.73), benzene (OR=1.50, 95% CI 1.08, 2.09), and three other Toxics related to fuel combustion. Risk of AML was increased with 3rd trimester exposure to chloroform (OR=1.30, 95% CI 1.00, 1.69), benzene (1.75, 95% CI 1.04, 2.93), and two other traffic-related Toxics. During the child's first year, exposure to butadiene, ortho-xylene, and toluene increased risk for AML and exposure to selenium increased risk for ALL. Benzene is an established cause of leukemia in adults; this study supports that ambient exposures to this and other chemicals in pregnancy and early life may also increase leukemia risk in children.

  • an exploratory study of ambient Air Toxics exposure in pregnancy and the risk of neuroblastoma in offspring
    Environmental Research, 2013
    Co-Authors: Julia E Heck, Myles Cockburn, Andrew S Park, Jiaheng Qiu, Beate Ritz
    Abstract:

    Little is known about the etiology of neuroblastoma, the most common cancer in infancy. In this study, we examined maternal exposure to ambient Air Toxics in pregnancy in relation to neuroblastoma in the child. We ascertained all cases of neuroblastoma listed in the California Cancer Registry 1990-2007 that could be linked to a California birth certificate, and controls were selected at random from California birth records. Average Air Toxics exposures during pregnancy were determined based upon measures from community-based Air pollution monitors. The study included 75 cases and 14,602 controls who lived with 5 km of an Air pollution monitor, and we additionally examined results for those living within a smaller radius around the monitor (2.5 km). Logistic regression was used to determine the risk of neuroblastoma with one interquartile range increase in Air toxic exposure. Neuroblastoma risk was increased with higher maternal exposure to carbon tetrachloride (OR=2.65, 95%CI 1.07, 6.53) and polycyclic aromatic hydrocarbons (OR=1.39, 95%CI 1.05, 1.84), particularly indeno(1,2,3-cd)pyrene and dibenz(a,h)anthracene. Hexavalent chromium was associated with neuroblastoma at the 5 km distance (OR=1.32, 95%CI 1.00, 1.74) but not at the 2.5 km distance. This is one of the first studies to report associations between neuroblastoma and these Air Toxics.

Allen L. Robinson - One of the best experts on this subject based on the ideXlab platform.

  • Evaluating the national Air Toxics assessment (NATA): Comparison of predicted and measured Air Toxics concentrations, risks, and sources in Pittsburgh, Pennsylvania
    Atmospheric Environment, 2011
    Co-Authors: Jennifer M. Logue, Mitchell J. Small, Allen L. Robinson
    Abstract:

    Abstract The National Air Toxics Assessment (NATA) is an ongoing modeling effort by the Environmental Protection Agency to predict Air Toxics concentrations, sources, and risks at the census tract level throughout the continental United States. To evaluate NATA, archived data collected at seven sites in and around Pittsburgh, Pennsylvania were compared to 2002 NATA predictions. The sites represent 3 different source regimes (mobile dominated, industrial point source dominated, and background). The evaluation considered 49 Air Toxics (37 gas-phase organics, 10 metals, coke oven emissions and diesel particulate matter); NATA’s performance was judged based on model-measurement comparisons of concentrations, health risks, and source contributions. On a concentration basis, NATA performance varied widely ranging from excellent for carbon tetrachloride to differences of more than a factor of 100 for low concentration chlorinated compounds. However, predicted concentrations were generally within a factor of 2 of measured values for Air Toxics that were estimated to be the primary cancer risk drivers; therefore NATA provided reasonable estimates of the additive cancer risks and risk ranking of Air Toxics. NATA performs better on average in Pittsburgh than nationwide. Comparison of source apportionment results indicates that NATA consistently underestimated concentrations of compounds emitted by large point sources as well as concentrations of chlorinated compounds, but overestimated the risks from mobile sources in Pittsburgh. Therefore, in Pittsburgh, NATA sufficiently prioritizes Air Toxics that drive potential cancer risks, but does not identify the sources of these priority Air Toxics.

  • spatial variation in ambient Air Toxics concentrations and health risks between industrial influenced urban and rural sites
    Journal of The Air & Waste Management Association, 2010
    Co-Authors: Jennifer M. Logue, Mitchell J. Small, Darrell Stern, Jason Maranche, Allen L. Robinson
    Abstract:

    Abstract Concentrations of 38 gas-phase organic Air Toxics were measured over a 2-yr period at four different sites in and around Pittsburgh, PA, to investigate spatial variations in health risks from chronic exposure. The sites were chosen to represent different exposure regimes: a downtown site with substantial mobile source emissions; two residential sites adjacent to one of the most heavily industrialized zones in Pittsburgh; and a regional background site. Lifetime cancer risks and non-cancer hazard quotients were estimated using a traditional and interactive risk models. Although study average concentrations of specific Air Toxics varied by as a much as a factor of 26 between the sites, the additive cancer risks of the gas-phase organic Air Toxics varied by less than a factor of 2, ranging from 6.1 × 10-5 to 9.5 × 10-5. The modest variation in risks reflects the fact that two regionally distributed Toxics, formalde-hyde and carbon tetrachloride (CCl4), contributed more than half of the cancer risk a...

  • high time resolved measurements of organic Air Toxics in different source regimes
    Atmospheric Environment, 2009
    Co-Authors: Jennifer M. Logue, K Huffhartz, Andrew T Lambe, Neil M Donahue, Allen L. Robinson
    Abstract:

    Abstract High time-resolved (HTR) measurements can provide significant insight into sources and exposures of Air pollution. In this study, an automated instrument was developed and deployed to measure hourly concentrations of 18 gas-phase organic Air Toxics and 6 volatile organic compounds (VOCs) at three sites in and around Pittsburgh, Pennsylvania. The sites represent different source regimes: a site with substantial mobile-source emissions; a residential site adjacent to a heavily industrialized zone; and an urban background site. Despite the close proximity of the sites (less than 13 km apart), the temporal characteristic of outdoor concentrations varied widely. Most of the compounds measured were characterized by short periods of elevated concentrations or plume events, but the duration, magnitude and composition of these events varied from site to site. The HTR data underscored the strong role of emissions from local sources on exposure to most Air Toxics. Plume events contributed more than 50% of the study average concentrations for all pollutants except chloroform, 1,2-dichloroethane, and carbon tetrachloride. Wind directional dependence of Air toxic concentrations revealed that emissions from large industrial facilities affected concentrations at all of the sites. Diurnal patterns and weekend/weekday variations indicated the effects of the mixing layer, point source emissions patterns, and mobile source Air Toxics (MSATs) on concentrations. Concentrations of many Air Toxics were temporally correlated, especially MSATs, indicating that they are likely co-emitted. It was also shown that correlations of the HTR data were greater than lower time resolution data (24-h measurements). This difference was most pronounced for the chlorinated pollutants. The stronger correlations in HTR measurements underscore their value for source apportionment studies.

  • identifying priority pollutant sources apportioning Air Toxics risks using positive matrix factorization
    Environmental Science & Technology, 2009
    Co-Authors: Jennifer M. Logue, Mitchell J. Small, Allen L. Robinson
    Abstract:

    Hazardous Air pollutants or Air Toxics are pollutants that are known or suspected to cause serious health effects. This paper presents a methodology to quantify source contributions to Air Toxics health risks. First, a linear, no-threshold risk model was used to identify gas-phase organic Air Toxics that contribute significantly to cancer risks. Next, Positive Matrix Factorization (PMF) was performed on high time-resolved measurements of these Air Toxics, and the additive cancer risks associated with each factor was determined. Finally, the PMF factors were linked to sources and source classes (mobile, nonmobile, secondary/background) using a combination of meteorological data and comparisons with published source profiles. The analysis was performed using data from three sites in Pittsburgh, Pennsylvania: a downtown site near a heavily traveled bus route, a residential site adjacent to a heavily industrialized area, and an urban background site. At all three sites emissions from nonmobile sources were the dominant contributors to the cancer risks from Air Toxics included in the PMF model, including benzene and other Air Toxics often associated with mobile source emissions. Emissions from both large industrial sources, such as coke works and chemical facilities, and smaller point sources, such as dry cleaners, contributed significantly to the cancer risks at all sites. This method can provide insight for decision makers to prioritize sources for risk reduction.

Elaine Symanski - One of the best experts on this subject based on the ideXlab platform.

  • abstract ia10 neighborhood matters residential levels of Air Toxics and increased risk of early childhood acute lymphocytic leukemia
    Cancer Prevention Research, 2020
    Co-Authors: Elaine Symanski, Grace Tee P Lewis, Tingyu Chen, Wenyaw Chan, Dejian Lan
    Abstract:

    Background: The evidence of benzene and 1,3-butadiene as leukemogens in adults comes primarily from occupational epidemiologic studies. The major environmental sources of benzene and 1,3-butadiene, which are classified as hazardous Air pollutants by the U.S. Environmental Protection Agency (EPA), include vehicular exhaust and emissions from industrial facilities. Exposures to these pollutants during in utero and early life may play an etiologic role in childhood leukemia. Hence, we conducted a population-based case-control study (Symanski et al., Environmental Health 2016;15:70) to examine the role of residential levels of benzene and 1,3-butadiene in early childhood leukemia in a state that has an abundant number of petrochemical plants and extensive road traffic in and around urban areas. Methods: We identified cases of acute lymphocytic leukemia (ALL) diagnosed in children under age 5 years from the Texas Cancer Registry for the years 1995-2011 and linked cancer registry data, where possible, to birth records in the state. Using Texas birth certificates, we selected 10 controls per case, frequency matching by birth month and year to allow for the same potential for exposure. Geocoded maternal addresses at delivery were linked to the U.S. EPA’s National-Scale Air Toxics Assessment modeled census-tract level estimates of benzene and 1,3-butadiene in ambient Air. We evaluated maternal and infant characteristics that were available from birth certificates, along with neighborhood-level metrics of disadvantage, as potential confounders. We applied mixed-effects logistic regression models to evaluate associations between Air pollutants and childhood leukemia in single and copollutant models. Results: In single-pollutant models, adjusted odds ratios were elevated for infants whose mothers lived in census tracts with higher benzene and 1,3-butadiene levels. In adjusted models that included benzene and 1,3-butadiene together, odds of ALL remained elevated for 1,3-butadiene (medium-exposure group: OR=1.22, 95% CI: 1.00-1.50; medium-high group: OR=1.28, 95% CI: 1.01-1.63; and high-exposure group: OR=1.40, 95% CI: 1.06-1.86) relative to the low-exposure group. In contrast, results were close to the null value for benzene in all exposure groups. Conclusions: Studies are needed to confirm our finding that early life environmental exposure to 1,3-butadiene (and not benzene) increases risk of ALL in young children. Our results add to the growing literature that health disparities arise, in part, because Air quality varies depending on where individuals live. Citation Format: Elaine Symanski, P. Grace Tee Lewis, Ting-Yu Chen, Wenyaw Chan, Dejian Lan, Xiaomei Ma. Neighborhood matters: Residential levels of Air Toxics and increased risk of early childhood acute lymphocytic leukemia [abstract]. In: Proceedings of the AACR Special Conference on Environmental Carcinogenesis: Potential Pathway to Cancer Prevention; 2019 Jun 22-24; Charlotte, NC. Philadelphia (PA): AACR; Can Prev Res 2020;13(7 Suppl): Abstract nr IA10.

  • Air Toxics and early childhood acute lymphocytic leukemia in texas a population based case control study
    Environmental Health, 2016
    Co-Authors: Elaine Symanski, Grace Tee P Lewis, Tingyu Chen, Wenyaw Chan, Dejian Lai
    Abstract:

    Traffic exhaust, refineries and industrial facilities are major sources of Air Toxics identified by the U.S. Environmental Protection Agency (U.S. EPA) for their potential risk to human health. In utero and early life exposures to Air Toxics such as benzene and 1,3-butadiene, which are known leukemogens in adults, may play an etiologic role in childhood leukemia that comprises the majority of pediatric cancers. We conducted a population based case–control study to examine individual effects of benzene, 1,3-butadiene and polycyclic organic matter (POM) in ambient residential Air on acute lymphocytic leukemia (ALL) diagnosed in children under age 5 years in Texas from 1995–2011. Texas Cancer Registry cases were linked to birth records and then were frequency matched by birth month and year to 10 population-based controls. Maternal and infant characteristics from birth certificates were abstracted to obtain information about potential confounders. Modelled estimates of benzene, 1,3-butadiene and POM exposures at the census tract level were assigned by linking geocoded maternal addresses from birth certificates to U.S. EPA National-Scale Air Toxics Assessment data for single and co-pollutant statistical analyses. Mixed-effects logistic regression models were applied to evaluate associations between Air Toxics and childhood leukemia. In adjusted single pollutant models, odds of childhood leukemia among mothers with the highest ambient Air exposures compared to those in the lowest quartile were 1.11 (95 % CI: 0.94–1.32) for POM, 1.17 (95 % CI: 0.98–1.39) for benzene and 1.29 (95 % CI: 1.08–1.52) for 1,3-butadiene. In co-pollutant models, odds ratios for childhood leukemia remained elevated for 1,3-butadiene but were close to the null value for benzene and POM. We observed positive associations between 1,3-butadiene and childhood leukemia in single and co-pollutant models whereas effect estimates from single pollutant models were diminished for benzene and POM in co-pollutant models. Early life exposure to 1,3-butadiene rather than benzene or POM appears to increase early childhood risk of acute lymphocytic leukemia.