Sonoma Technology Inc.

Petaluma, CA, United States

Sonoma Technology Inc.

Petaluma, CA, United States
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Volk H.E.,University of Southern California | Lurmann F.,Sonoma Technology Inc. | Penfold B.,Sonoma Technology Inc. | Hertz-Picciotto I.,University of California at Davis | McConnell R.,University of Southern California
Archives of General Psychiatry | Year: 2013

Context: Autism is a heterogeneous disorder with genetic and environmental factors likely contributing to its origins. Examination of hazardous pollutants has suggested the importance of air toxics in the etiology of autism, yet little research has examined its association with local levels of air pollution using residence-specific exposure assignments. Objective: To examine the relationship between trafficrelated air pollution, air quality, and autism. Design : This population-based case-control study includes data obtained from children with autism and control children with typical development who were enrolled in the Childhood Autism Risks from Genetics and the Environment study in California. The mother's address from the birth certificate and addresses reported from a residential history questionnaire were used to estimate exposure for each trimester of pregnancy and first year of life. Traffic-related air pollution was assigned to each location using a line-source air-quality dispersion model. Regional air pollutant measures were based on the Environmental Protection Agency's Air Quality System data. Logistic regression models compared estimated and measured pollutant levels for children with autism and for control children with typical development. Setting: Case-control study from California. Participants: A total of 279 children with autism and a total of 245 control children with typical development. Main Outcome Measures: Crude and multivariable adjusted odds ratios (AORs) for autism. Results: Children with autism were more likely to live at residences that had the highest quartile of exposure to traffic-related air pollution, during gestation (AOR, 1.98 [95% CI, 1.20-3.31]) and during the first year of life (AOR, 3.10 [95% CI, 1.76-5.57]), compared with control children. Regional exposure measures of nitrogen dioxide and particulate matter less than 2.5 and 10 μm in diameter (PM2.5 and PM10) were also associated with autism during gestation (exposure to nitrogen dioxide: AOR, 1.81 [95% CI, 1.37-3.09]; exposure to PM 2.5: AOR, 2.08 [95% CI, 1.93-2.25]; exposure to PM10: AOR, 2.17 [95% CI, 1.49-3.16) and during the first year of life (exposure to nitrogen dioxide: AOR, 2.06 [95% CI, 1.37-3.09]; exposure to PM2.5: AOR, 2.12 [95% CI, 1.45-3.10]; exposure to PM10: AOR, 2.14 [95% CI, 1.46-3.12]). All regional pollutant estimates were scaled to twice the standard deviation of the distribution for all pregnancy estimates. Conclusions: Exposure to traffic-related air pollution, nitrogen dioxide, PM2.5, and PM10 during pregnancy and during the first year of life was associated with autism. Further epidemiological and toxicological examinations of likely biological pathways will help determine whether these associations are causal. ©2013 American Medical Association. All rights reserved.

Volk H.E.,University of Southern California | Kerin T.,University of Southern California | Lurmann F.,Sonoma Technology Inc. | Hertz-Picciotto I.,University of California at Davis | And 3 more authors.
Epidemiology | Year: 2014

BACKGROUND:: Independent studies report association of autism spectrum disorder with air pollution exposure and a functional promoter variant (rs1858830) in the MET receptor tyrosine kinase (MET) gene. Toxicological data find altered brain Met expression in mice after prenatal exposure to a model air pollutant. Our objective was to investigate whether air pollution exposure and MET rs1858830 genotype interact to alter the risk of autism spectrum disorder. METHODS:: We studied 252 cases of autism spectrum disorder and 156 typically developing controls from the Childhood Autism Risk from Genetics and the Environment Study. Air pollution exposure was assigned for local traffic-related sources and regional sources (particulate matter, nitrogen dioxide, and ozone). MET genotype was determined by direct resequencing. RESULTS:: Subjects with both MET rs1858830 CC genotype and high air pollutant exposures were at increased risk of autism spectrum disorder compared with subjects who had both the CG/GG genotypes and lower air pollutant exposures. There was evidence of multiplicative interaction between NO2 and MET CC genotype (P= 0.03). CONCLUSIONS:: MET rs1858830 CC genotype and air pollutant exposure may interact to increase the risk of autism spectrum disorder. Copyright © 2013 by Lippincott Williams & Wilkins.

Volk H.E.,University of Southern California | Hertz-Picciotto I.,University of California at Davis | Delwiche L.,University of California at Davis | Lurmann F.,Sonoma Technology Inc | McConnell R.,University of Southern California
Environmental Health Perspectives | Year: 2011

Background: Little is known about environmental causes and contributing factors for autism. Basic science and epidemiologic research suggest that oxidative stress and inflammation may play a role in disease development. Traffic-related air pollution, a common exposure with established effects on these pathways, contains substances found to have adverse prenatal effects. Objectives: We examined the association between autism and proximity of residence to freeways and major roadways during pregnancy and near the time of delivery, as a surrogate for air pollution exposure. Methods: Data were from 304 autism cases and 259 typically developing controls enrolled in the Childhood Autism Risks from Genetics and the Environment (CHARGE) study. The mother's address recorded on the birth certificate and trimester-specific addresses derived from a residential history obtained by questionnaire were geocoded, and measures of distance to freeways and major roads were calculated using ArcGIS software. Logistic regression models compared residential proximity to freeways and major roads for autism cases and typically developing controls. Results: Adjusting for sociodemographic factors and maternal smoking, maternal residence at the time of delivery was more likely be near a freeway (≤ 309 m) for cases than for controls [odds ratio (OR) = 1.86; 95% confidence interval (CI), 1.04-3.45]. Autism was also associated with residential proximity to a freeway during the third trimester (OR = 2.22; CI, 1.16-4.42). After adjustment for socioeconomic and sociodemographic characteristics, these associations were unchanged. Living near other major roads at birth was not associated with autism. Conclusions: Living near a freeway was associated with autism. Examination of associations with measured air pollutants is needed.

Valin L.C.,University of California at Berkeley | Valin L.C.,Sonoma Technology Inc | Russell A.R.,University of California at Berkeley | Cohen R.C.,University of California at Berkeley
Geophysical Research Letters | Year: 2013

The evolution of atmospheric composition downwind of a city depends strongly on the concentration of OH within the plume. We use space-based observations of NO2, a molecule that affects both the sources and sinks of OH, to examine the functional dependence of OH concentration on the speed of the wind over Riyadh, Saudi Arabia. These observations illustrate the nonlinear dependence of the OH concentration on NO2 and on the rate of atmospheric mixing. We derive a range of NOx lifetimes of 5.5-8.0 h, lifetimes that correspond to an effective plume-averaged OH concentration of 7.6 × 106 molecules cm-3 at fast (26 km h -1) and 5.2 × 106 molecules cm-3 at slow (4 km h-1) wind speeds. Key PointsThe lifetime of NOx depends on the wind speedNO2 spatial patterns depend on wind speedInferring the NOx lifetime from space requires spatially-detailed measurements ©2013. American Geophysical Union. All Rights Reserved.

Brandt S.J.,University of Massachusetts Amherst | Perez L.,Swiss Tropical and Public Health Institute | Kunzli N.,Swiss Tropical and Public Health Institute | Lurmannp F.,Sonoma Technology Inc. | McConnell R.,University of Southern California
European Respiratory Journal | Year: 2012

Recent research suggests the burden of childhood asthma that is attributable to air pollution has been underestimated in traditional risk assessments, and there are no estimates of these associated costs. We aimed to estimate the yearly childhood asthma-related costs attributable to air pollution for Riverside and Long Beach, CA, USA, including: 1) the indirect and direct costs of healthcare utilisation due to asthma exacerbations linked with traffic-related pollution (TRP); and 2) the costs of health care for asthma cases attributable to local TRP exposure. We calculated costs using estimates from peer-reviewed literature and the authors' analysis of surveys (Medical Expenditure Panel Survey, California Health Interview Survey, National Household Travel Survey, and Health Care Utilization Project). A lower-bound estimate of the asthma burden attributable to air pollution was US$18 million yearly. Asthma cases attributable to TRP exposure accounted for almost half of this cost. The cost of bronchitic episodes was a major proportion of both the annual cost of asthma cases attributable to TRP and of pollution-linked exacerbations. Traditional risk assessment methods underestimate both the burden of disease and cost of asthma associated with air pollution, and these costs are borne disproportionately by communities with higher than average TRP. Copyright©ERS 2012.

McConnell R.,University of Southern California | Shen E.,University of Southern California | Gilliland F.D.,University of Southern California | Jerrett M.,University of California at Berkeley | And 4 more authors.
Environmental Health Perspectives | Year: 2015

Background: Childhood body mass index (BMI) and obesity prevalence have been associated with exposure to secondhand smoke (SHS), maternal smoking during pregnancy, and vehicular air pollution. There has been little previous study of joint BMI effects of air pollution and tobacco smoke exposure. Methods: Information on exposure to SHS and maternal smoking during pregnancy was collected on 3,318 participants at enrollment into the Southern California Children’s Health Study. At study entry at average age of 10 years, residential near-roadway pollution exposure (NRP) was estimated based on a line source dispersion model accounting for traffic volume, proximity, and meteorology. Lifetime exposure to tobacco smoke was assessed by parent questionnaire. Associations with subsequent BMI growth trajectory based on annual measurements and attained BMI at 18 years of age were assessed using a multilevel modeling strategy. results: Maternal smoking during pregnancy was associated with estimated BMI growth over 8-year follow-up (0.72 kg/m2 higher; 95% CI: 0.14, 1.31) and attained BMI (1.14 kg/m2 higher; 95% CI: 0.66, 1.62). SHS exposure before enrollment was positively associated with BMI growth (0.81 kg/m2 higher; 95% CI: 0.36, 1.27) and attained BMI (1.23 kg/m2 higher; 95% CI: 0.86, 1.61). Growth and attained BMI increased with more smokers in the home. Compared with children without a history of SHS and NRP below the median, attained BMI was 0.80 kg/m2 higher (95% CI: 0.27, 1.32) with exposure to high NRP without SHS; 0.85 kg/m2 higher (95% CI: 0.43, 1.28) with low NRP and a history of SHS; and 2.15 kg/m2 higher (95% CI: 1.52, 2.77) with high NRP and a history of SHS (interaction p-value 0.007). These results suggest a synergistic effect. conclusions: Our findings strengthen emerging evidence that exposure to tobacco smoke and NRP contribute to development of childhood obesity and suggest that combined exposures may have synergistic effects. © 2015, Public Health Services, US Dept of Health and Human Services. All rights reserved

Field R.A.,University of Wyoming | Soltis J.,University of Wyoming | McCarthy M.C.,Sonoma Technology Inc. | Murphy S.,University of Wyoming | Montague D.C.,University of Wyoming
Atmospheric Chemistry and Physics | Year: 2015

Emissions from oil and natural gas development during winter in the Upper Green River basin of Wyoming are known to drive episodic ozone (O3/ production. Contrasting O3 distributions were observed in the winters of 2011 and 2012, with numerous episodes (hourly O3 ≥85 ppbv) in 2011 compared to none in 2012. The lack of O3 episodes in 2012 coincided with a reduction in measured ambient levels of total non-methane hydrocarbons (NMHC). Measurements of speciated NMHC, and other air quality parameters, were performed to better understand emission sources and to determine which compounds are most active in promoting O3 formation. Positive matrix factorization (PMF) analyses of the data were carried out to help achieve these goals. PMF analyses revealed three contributing factors that were identified with different emission source types: factor 1, combustion/traffic; factor 2, fugitive natural gas; and factor 3, fugitive condensate. Compositional signatures of the three contributing factors were identified through comparison with independently derived emission source profiles. Fugitive emissions of natural gas and of condensate were the two principal emission source types for NMHC. A water treatment and recycling facility was found to be a significant source of NMHC that are abundant in condensate, in particular toluene and m+p-xylene. Emissions from water treatment have an influence upon peak O3 mixing ratios at downwind measurement sites. © 2015 Author(s). CC Attribution 3.0 License.

Salam M.T.,University of Southern California | Byun H.-M.,Harvard University | Lurmann F.,Sonoma Technology Inc. | Breton C.V.,University of Southern California | And 3 more authors.
Journal of Allergy and Clinical Immunology | Year: 2012

Background: Inducible nitric oxide synthase (iNOS; encoded by nitric oxide synthase isoform 2 [NOS2]) is the major enzyme for nitric oxide synthesis in airways. As such, measurement of fractional concentration of exhaled nitric oxide (Feno) provides an in vivo assessment of iNOS activity. Short-term exposure to air pollution, haplotypes, and DNA methylation in the NOS2 promoter has been associated independently with iNOS expression, Feno levels, or both. Objective: We aimed to examine the effects of ambient air pollutants, NOS2 promoter haplotypes, and NOS2 promoter methylation on Feno levels in children. Methods: We selected 940 participants in the Children's Health Study who provided buccal samples and had undergone Feno measurement on the same day. DNA methylation was measured with a bisulfite-PCR Pyrosequencing assay. Seven single nucleotide polymorphisms captured the haplotype diversity in the NOS2 promoter. Average particulate matter with an aerodynamic diameter of 2.5 μm or less (PM 2.5) and 10 μm (PM 10) or less and ozone and nitrogen dioxide levels 7 days before Feno measurement were estimated based on air pollution data obtained at central monitoring sites. Results: We found interrelated effects of PM 2.5, NOS2 promoter haplotypes, and iNOS methylation on Feno levels. Increased 7-day average PM 2.5 exposure was associated with lower iNOS methylation (P =.01). NOS2 promoter haplotypes were globally associated with NOS2 promoter methylation (P = 6.2 × 10 -8). There was interaction among 1 common promoter haplotype, iNOS methylation level, and PM 2.5 exposure on Feno levels (P interaction =.00007). Conclusion: Promoter variants in NOS2 and short-term PM 2.5 exposure affect iNOS methylation. This is one of the first studies showing contributions of genetic and epigenetic variations in air pollution-mediated phenotype expression. © 2011 American Academy of Allergy, Asthma & Immunology.

Russell A.R.,University of California at Berkeley | Russell A.R.,Sonoma Technology Inc. | Valin L.C.,University of California at Berkeley | Cohen R.C.,University of California at Berkeley
Atmospheric Chemistry and Physics | Year: 2012

Observations of tropospheric NO2 vertical column densities over the United States (US) for 2005-2011 are evaluated using the OMI Berkeley High Resolution (BEHR) retrieval algorithm. We assess changes in NO2 on day-of-week and interannual timescales to assess the impact of changes in emissions from mobile and non-mobile sources on the observed trends. We observe consistent decreases in cities across the US, with an average total reduction of 32 ± 7% across the 7 yr. Changes for large power plants have been more variable (-26 ± 12%) due to regionally-specific regulation policies. An increasing trend of 10-20% in background NO2 columns in the northwestern US is observed. We examine the impact of the economic recession on emissions and find that decreases in NO2 column densities over cities were moderate prior to the recession (-6 ± 5% yr−1), larger during the recession (-8 ± 5% yr−1), and then smaller after the recession (-3 ± 4% yr−1). Differences in the trends observed on weekdays and weekends indicate that prior to the economic recession, NO2 reductions were dominated by technological improvements to the light-duty vehicle fleet but that a decrease in diesel truck activity has contributed to emission reductions since the recession. We use the satellite observations to estimate a 34% decrease in NO2 from mobile sources in cities for 2005-2011 and use that value to infer changes in non-mobile sources. We find that reductions in NO2 from non-mobile sources in cities have been both more modest and more variable than NO 2 reductions from mobile sources (-10 ± 13%). © 2012 Author(s).

Urman R.,University of Southern California | McConnell R.,University of Southern California | Islam T.,University of Southern California | Avol E.L.,University of Southern California | And 6 more authors.
Thorax | Year: 2014

Background Previous studies have reported adverse effects of either regional or near-roadway air pollution (NRAP) on lung function. However, there has been littlestudy of the joint effects of these exposures. Objectives To assess the joint effects of NRAP and regional pollutants on childhood lung function in the Children's Health Study. Methods Lung function was measured on 1811 children from eight Southern Californian communities. NRAP exposure was assessed based on (1) residential distance to the nearest freeway or major road and (2) estimated near-roadway contributions to residential nitrogen dioxide (NO2), nitric oxide (NO) and total nitrogen oxides (NOx). Exposure to regional ozone (O3), NO2, particulate matter with aerodynamic diameter <10 μm (PM10) and 2.5 μm (PM 2.5) was measured continuously at community monitors. Results An increase in near-roadway NOx of 17.9 ppb (2 SD) was associated with deficits of 1.6% in forced vital capacity (FVC) (p=0.005) and 1.1% in forced expiratory volume in 1 s (FEV1) ( p=0.048). Effects were observed in all communities and were similar for NO2 and NO. Residential proximity to a freeway was associated with a reduction in FVC. Lung function deficits of 2-3% were associated with regional PM10 and PM2.5 (FVC and FEV1) and with O3 (FEV1), but not NO2 across the range of exposure between communities. Associations with regional pollution and NRAP were independent in models adjusted for each. The effects of NRAP were not modified by regional pollutant concentrations. Conclusions The results indicate that NRAP and regional air pollution have independent adverse effects on childhood lung function.

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