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BACKGROUND:Among U.S. residents, tuberculosis (TB) disease disproportionally affects non-U.S.-born persons and varies substantially by country of birth. Yet TB disease incidence rates by country of birth are not routinely reported despite these large, known health disparities. This is in part due to the technical challenges of using standard regression analysis with a communicable disease. Here, we estimate tuberculosis disease incidence rates by country of birth and demonstrate methods for overcoming these challenges using TB surveillance data from Los Angeles County which has more than 3.5 million non-U.S.-born residents. METHODS:Cross-sectional data on 5,447 cases of TB disease from Los Angeles County were combined with population estimates from the American Community Survey to calculate TB disease incidence rates for 2005 through 2011. Adjusted incidence rates were modelled using Poisson and negative binomial regressions. Bayesian models were used to account for the uncertainty in population estimates. RESULTS:The unadjusted incidence rate among non-U.S.-born persons was 15 per 100,000 person-years in contrast to the rate among U.S-born persons, 2 per 100,000. The unadjusted incidence rates were 44 and 12 per 100,000 person-years among persons born in the Philippines and Mexico, respectively. In adjusted analysis, persons born in the Philippines were 2.6 (95% CI: 2.3-3.1) times as likely to be reported as a TB case than persons born in Mexico. Bayesian models showed similar results. CONCLUSION:This study confirms substantial disparities in TB disease by country of birth in Los Angeles County. Accounting for age, gender, years in residence and year of diagnosis, persons from the Philippines, Vietnam and several other countries had much higher rates of reported TB disease than other foreign countries. We demonstrated that incidence rates by country of birth can be estimated using available data despite technical challenges.

Prenatal psychosocial stressors may increase the risk of wheeze in young offspring, yet little attention has been given to the effects that maternal ethnicity may have on this relationship. From a population-based cohort of 1193 children, we assessed the effect of maternal prenatal stressors on the risk of lifetime wheeze in young offspring. We further studied whether maternal Latina ethnicity modified these associations. The risk of wheeze in the offspring was increased from high levels of pregnancy anxiety (aRR 1.40, 95 % CI 1.07, 1.83), negative life events (aRR 1.36, 95 % CI 1.06, 1.75), or low paternal support (aRR 1.41, 95 % CI 1.02, 1.96). The risk of lifetime wheeze was stronger in the offspring of Latina mothers than of White mothers for these same stressors. Multiple maternal prenatal stressors are associated with increased risk of lifetime wheeze in young offspring, with slight effect modification by Latina ethnicity.

Exposure to air pollution during pregnancy has been linked to the risk of childhood cancer, but the evidence remains inconclusive. In the present study, we used land use regression modeling to estimate prenatal exposures to traffic exhaust and evaluate the associations with cancer risk in very young children. Participants in the Air Pollution and Childhood Cancers Study who were 5 years of age or younger and diagnosed with cancer between 1988 and 2008 were had their records linked to California birth certificates, and controls were selected from birth certificates. Land use regression-based estimates of exposures to nitric oxide, nitrogen dioxide, and nitrogen oxides were assigned based on birthplace residence and temporally adjusted using routine monitoring station data to evaluate air pollution exposures during specific pregnancy periods. Logistic regression models were adjusted for maternal age, race/ethnicity, educational level, parity, insurance type, and Census-based socioeconomic status, as well as child's sex and birth year. The odds of acute lymphoblastic leukemia increased by 9%, 23%, and 8% for each 25-ppb increase in average nitric oxide, nitrogen dioxide, and nitrogen oxide levels, respectively, over the entire pregnancy. Second- and third-trimester exposures increased the odds of bilateral retinoblastoma. No associations were found for annual average exposures without temporal components or for any other cancer type. These results lend support to a link between prenatal exposure to traffic exhaust and the risk of acute lymphoblastic leukemia and bilateral retinoblastoma.

BackgroundNumerous studies have linked criteria air pollutants with adverse birth outcomes, but there is less information on the importance of specific emission sources, such as traffic, and air toxics.ObjectivesWe used three exposure data sources to examine odds of term low birth weight (LBW) in Los Angeles, California, women when exposed to high levels of traffic-related air pollutants during pregnancy.MethodsWe identified term births during 1 June 2004 to 30 March 2006 to women residing within 5 miles of a South Coast Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. Pregnancy period average exposures were estimated for air toxics, including polycyclic aromatic hydrocarbons (PAHs), source-specific particulate matter < 2.5 μm in aerodynamic diameter (PM2.5) based on a chemical mass balance model, criteria air pollutants from government monitoring data, and land use regression (LUR) model estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of term LBW (< 2,500 g) were examined using logistic regression.ResultsOdds of term LBW increased approximately 5% per interquartile range increase in entire pregnancy exposures to several correlated traffic pollutants: LUR measures of NO, NO2, and NOx, elemental carbon, and PM2.5 from diesel and gasoline combustion and paved road dust (geological PM2.5).ConclusionsThese analyses provide additional evidence of the potential impact of traffic-related air pollution on fetal growth. Particles from traffic sources should be a focus of future studies.

Abstract Background Numerous studies have associated air pollutant exposures with adverse birth outcomes, but there is still relatively little information to attribute effects to specific emission sources or air toxics. We used three exposure data sources to examine risks of preterm birth in Los Angeles women when exposed to high levels of traffic-related air pollutants - including specific toxics - during pregnancy. Methods We identified births during 6/1/04-3/31/06 to women residing within five miles of a Southern California Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. We identified preterm cases and, using a risk set approach, matched cases to controls based on gestational age at birth. Pregnancy period exposure averages were estimated for a number of air toxics including polycyclic aromatic hydrocarbons (PAHs), source-specific PM2.5 (fine particulates with aerodynamic diameter less than 2.5 μm) based on a Chemical Mass Balance model, criteria air pollutants based on government monitoring data, and land use regression (LUR) estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of preterm birth were estimated using conditional logistic regression. Results Odds of preterm birth increased 6-21% per inter-quartile range increase in entire pregnancy exposures to organic carbon (OC), elemental carbon (EC), benzene, and diesel, biomass burning and ammonium nitrate PM2.5, and 30% per inter-quartile increase in PAHs; these pollutants were positively correlated and clustered together in a factor analysis. Associations with LUR exposure metrics were weaker (3-4% per inter-quartile range increase). Conclusions These latest analyses provide additional evidence of traffic-related air pollution's impact on preterm birth for women living in Southern California and indicate PAHs as a pollutant of concern that should be a focus of future studies. Other PAH sources besides traffic were also associated with higher odds of preterm birth, as was ammonium nitrate PM2.5, the latter suggesting potential importance of secondary pollutants. Future studies should focus on accurate modeling of both local and regional spatial and temporal distributions, and incorporation of source information.

Maternal psychosocial stress is an important risk factor for preterm birth, but support interventions have largely been unsuccessful. The objective of this study is to assess how support during pregnancy influences preterm birth risk and possibly ameliorates the effects of chronic stress, life event stress, or pregnancy anxiety in pregnant women. We examined 1,027 singleton preterm births and 1,282 full-term normal weight controls from a population-based retrospective case–control study of Los Angeles County, California women giving birth in 2003, a mostly Latina population (both US-born and immigrant). We used logistic regression to assess whether support from the baby’s father during pregnancy influences birth outcomes and effects of chronic stress, pregnancy anxiety, and life event stress. Adjusted odds of preterm birth decreased with better support (OR 0.73 [95%CI 0.52, 1.01]). Chronic stress (OR 1.46 [95%CI 1.11, 1.92]), low confidence of a normal birth (OR 1.57 [95% CI 1.17, 2.12]), and fearing for the baby’s health (OR 1.67 [95%CI 1.30, 2.14]) increased preterm birth risk, but life events showed no association. Our data also suggested that paternal support may modify the effect of chronic stress on the risk of preterm birth, such that among mothers lacking support, those with moderate-to-high stress were at increased odds of delivering preterm (OR 2.15 [95%CI 0.92, 5.03]), but women with greater support had no increased risk with moderate-to-high chronic stress (OR 1.13 [95%CI 0.94, 1.35]). Paternal support may moderate the effects of chronic stress on the risk of preterm delivery.

Ambient particulate matter (PM2.5) is an important component of natural and human-generated air pollution and a major contributor to the global burden of disease. Short-term effects of PM2.5 exposure on respiratory illness have been described but most evidence arises from high pollution settings. We used case-crossover methods to estimate effects of outdoor PM2.5 levels on emergency department (ED) presentations and hospital admissions for a range of acute respiratory illnesses and age groups in Melbourne, Australia from 2014–2019, with and without adjustment for other pollutants and weather conditions, using daily and one-week averaged lags. We estimated incidence rate ratios for a 10 μg/m3 increase in 7-day average ambient PM2.5 of 1.043 (95% confidence interval (CI): 1.000–1.089) on ED presentation and 1.013 (95% CI: 0.971–1.056) on hospital admissions for acute respiratory illnesses for patients of any age. We observed distinct temporal patterns in daily lag effect by disease. The largest effects on acute lower respiratory tract infection and asthma were observed in children. Ambient PM2.5 levels rarely exceeded standards in place at the time. Although uncertainty around most point estimates was relatively wide, these findings are most compatible with adverse health effects of ambient PM2.5 at levels below currently established Australian national standards.Implications: Understanding the health impacts of air pollution is important for setting air quality targets, as well as for informing robust health system planning. Adverse effects of exposure to outdoor fine particulate matter on human respiratory health have been consistently described. However, most studies have been done in higher-pollution settings. Further, many studies have assessed health effects in broad categories such as all-cause respiratory mortality or hospitalization, and thus lack the granularity to inform detailed health service planning. Our study aimed to estimate effects of outdoor fine particulate matter on emergency department (ED) presentations and hospital admissions for a range of acute respiratory illnesses and age groups in Melbourne, Australia, a city with relatively good air quality by international comparison. Our study estimated consistent effects on both ED presentations and hospital admissions compatible with distinct patterns of adverse health effects at levels at or below established Australian national (and many international) standards. These results will help to inform both air quality policy and public health policy in similar settings. [ABSTRACT FROM AUTHOR]

Abstract Background Numerous studies have associated air pollutant exposures with adverse birth outcomes, but there is still relatively little information to attribute effects to specific emission sources or air toxics. We used three exposure data sources to examine risks of preterm birth in Los Angeles women when exposed to high levels of traffic-related air pollutants - including specific toxics - during pregnancy. Methods We identified births during 6/1/04-3/31/06 to women residing within five miles of a Southern California Air Quality Management District (SCAQMD) Multiple Air Toxics Exposure Study (MATES III) monitoring station. We identified preterm cases and, using a risk set approach, matched cases to controls based on gestational age at birth. Pregnancy period exposure averages were estimated for a number of air toxics including polycyclic aromatic hydrocarbons (PAHs), source-specific PM2.5 (fine particulates with aerodynamic diameter less than 2.5 μm) based on a Chemical Mass Balance model, criteria air pollutants based on government monitoring data, and land use regression (LUR) estimates of nitric oxide (NO), nitrogen dioxide (NO2) and nitrogen oxides (NOx). Associations between these metrics and odds of preterm birth were estimated using conditional logistic regression. Results Odds of preterm birth increased 6-21% per inter-quartile range increase in entire pregnancy exposures to organic carbon (OC), elemental carbon (EC), benzene, and diesel, biomass burning and ammonium nitrate PM2.5, and 30% per inter-quartile increase in PAHs; these pollutants were positively correlated and clustered together in a factor analysis. Associations with LUR exposure metrics were weaker (3-4% per inter-quartile range increase). Conclusions These latest analyses provide additional evidence of traffic-related air pollution's impact on preterm birth for women living in Southern California and indicate PAHs as a pollutant of concern that should be a focus of future studies. Other PAH sources besides traffic were also associated with higher odds of preterm birth, as was ammonium nitrate PM2.5, the latter suggesting potential importance of secondary pollutants. Future studies should focus on accurate modeling of both local and regional spatial and temporal distributions, and incorporation of source information.

Ambient particulate matter (PM 2.5 ) is an important component of natural and human-generated air pollution and a major contributor to the global burden of disease. Short-term effects of PM 2.5 exposure on respiratory illness have been described but most evidence arises from high pollution settings. We used case-crossover methods to estimate effects of outdoor PM 2.5 levels on emergency department (ED) presentations and hospital admissions for a range of acute respiratory illnesses and age groups in Melbourne, Australia from 2014-2019, with and without adjustment for other pollutants and weather conditions, using daily and one-week averaged lags. We estimated incidence rate ratios for a 10 μg/m 3 increase in 7-day average ambient PM 2.5 of 1.043 (95% confidence interval (CI): 1.000-1.089) on ED presentation and 1.013 (95% CI: 0.971-1.056) on hospital admissions for acute respiratory illnesses for patients of any age. We observed distinct temporal patterns in daily lag effect by disease. The largest effects on acute lower respiratory tract infection and asthma were observed in children. Ambient PM 2.5 levels rarely exceeded standards in place at the time. Although uncertainty around most point estimates was relatively wide, these findings are most compatible with adverse health effects of ambient PM 2.5 at levels below currently established Australian national standards. Implications : Understanding the health impacts of air pollution is important for setting air quality targets, as well as for informing robust health system planning. Adverse effects of exposure to outdoor fine particulate matter on human respiratory health have been consistently described. However, most studies have been done in higher-pollution settings. Further, many studies have assessed health effects in broad categories such as all-cause respiratory mortality or hospitalization, and thus lack the granularity to inform detailed health service planning. Our study aimed to estimate effects of outdoor fine particulate matter on emergency department (ED) presentations and hospital admissions for a range of acute respiratory illnesses and age groups in Melbourne, Australia, a city with relatively good air quality by international comparison. Our study estimated consistent effects on both ED presentations and hospital admissions compatible with distinct patterns of adverse health effects at levels at or below established Australian national (and many international) standards. These results will help to inform both air quality policy and public health policy in similar settings.