Association between Airport Ultrafine Particles and Lung Cancer Risk: The Multiethnic Cohort Study.

BACKGROUND: Ultrafine particles (UFP) are unregulated air pollutants abundant in aviation exhaust. Emerging evidence suggests that UFPs may impact lung health due to their high surface area-to-mass ratio and deep penetration into airways. This study aimed to assess long-term exposure to airport-related UFPs and lung cancer incidence in a multiethnic population in Los Angeles County. METHODS: Within the California Multiethnic Cohort, we examined the association between long-term exposure to airport-related UFPs and lung cancer incidence. Multivariable Cox proportional hazards regression models were used to estimate the effect of UFP exposure on lung cancer incidence. Subgroup analyses by demographics, histology and smoking status were conducted. RESULTS: Airport-related UFP exposure was not associated with lung cancer risk [per one IGR HR, 1.01; 95% confidence interval (CI), 0.97-1.05] overall and across race/ethnicity. A suggestive positive association was observed between a one IQR increase in UFP exposure and lung squamous cell carcinoma (SCC) risk (HR, 1.08; 95% CI, 1.00-1.17) with a Phet for histology = 0.05. Positive associations were observed in 5-year lag analysis for SCC (HR, 1.12; 95% CI, CI, 1.02-1.22) and large cell carcinoma risk (HR, 1.23; 95% CI, 1.01-1.49) with a Phet for histology = 0.01. CONCLUSIONS: This large prospective cohort analysis suggests a potential association between airport-related UFP exposure and specific lung histologies. The findings align with research indicating that UFPs found in aviation exhaust may induce inflammatory and oxidative injury leading to SCC. IMPACT: These results highlight the potential role of airport-related UFP exposure in the development of lung SCC.

Spatial clusters of extended-spectrum beta-lactamase-producing Escherichia coli causing community-onset bacteriuria due to repeat infections: cluster analysis from a large urban medical center, San Francisco, 2014-2020.

BACKGROUND: Urinary tract infections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli (ESBL-E. coli) may occur as outbreaks due to common-source exposures. Yet, it is currently unknown if they cluster geographically as would be expected as part of an outbreak. METHODS: We collected electronic health record data on all patients living in San Francisco with culture-documented community-onset E. coli bacteriuria in a safety-net public healthcare system from January 2014 to March 2020 (diagnosed < 48 h after hospital admission or in outpatient clinical settings without a hospitalization in the past 90 days). We assessed the presence of spatial clusters of (1) ESBL-E. coli bacteriuria episodes, and (2) individuals with any ESBL-E. coli bacteriuria episode, with Global and Local Moran's I. We evaluated differences in prevalence of bacteriuria recurrence by ESBL-production by Poisson regression. RESULTS: Out of 4,304 unique individuals, we identified spatial clusters of ESBL-E. coli bacteriuria episodes (n = 461) compared to non-ESBL-E. coli bacteriuria episodes (n = 5477; Global Moran's p < 0.001). Spatial clusters of individuals with any bacteriuria caused by ESBL-E. coli were not identified (p = 0.43). Bacteriuria recurrence was more likely to occur with ESBL-E. coli (odds ratio [OR] 2.78, 95% confidence interval [95% CI] 2.10, 3.66, p < 0.001), particularly after an initial ESBL-E. coli bacteriuria episode (OR 2.27, 95% CI 1.82, 2.83, p < 0.001). CONCLUSION: We found spatial clusters of ESBL-E. coli bacteriuria episodes. However, this was partly explained by clustering within individuals more than between individuals, as having an ESBL-E. coli bacteriuria was associated with recurrence with ESBL-E. coli. These findings may help better tailor clinical treatment of patients with recurrent urinary tract infections after an initial episode caused by ESBL-E. coli.

Spatial clusters of extended-spectrum beta-lactamase-producing Escherichia coli causing community-onset bacteriuria due to repeat infections: cluster analysis from a large urban medical center, San Francisco, 2014-2020.

Background: Urinary tract infections caused by extended-spectrum beta-lactamase (ESBL)-producing Escherichia coli (ESBL-E. coli) may occur as outbreaks due to common-source exposures. Yet, it is currently unknown if they cluster geographically as would be expected as part of an outbreak. Methods: We collected electronic health record data on all patients living in San Francisco with culture-documented community-onset E. coli bacteriuria in a safety-net public healthcare system from January 2014 to March 2020 (diagnosed < 48 hours after hospital admission or in outpatient clinical settings without a hospitalization in the past 90 days). We assessed the presence of spatial clusters of (1) ESBL-E. coli bacteriuria episodes, and (2) individuals with any ESBL-E. coli bacteriuria episode, with Global and Local Moran's I. We evaluated differences in prevalence of bacteriuria recurrence by ESBL-production by Poisson regression. Results: Out of 4,304 unique individuals, we identified spatial clusters of ESBL-E. coli bacteriuria episodes (n = 461) compared to non-ESBL-E. coli bacteriuria episodes (n = 5477; Global Moran's p < 0.001). Spatial clusters of individuals with any bacteriuria caused by ESBL-E. coli were not identified (p = 0.43). Bacteriuria recurrence was more likely to occur with ESBL-E. coli (odds ratio [OR] 2.78, 95% confidence interval [95% CI] 2.10, 3.66, p < 0.001), particularly after an initial ESBL-E. coli bacteriuria episode (OR 2.27, 95% CI 1.82, 2.83, p < 0.001). Conclusion: We found spatial clusters of ESBL-E. coli bacteriuria episodes. However, this was partly explained by clustering within individuals more than between individuals, as having an ESBL-E. coli bacteriuria was associated with recurrence with ESBL-E. coli.

Role of neighborhood context in ovarian cancer survival disparities: current research and future directions.

Ovarian cancer is the fifth leading cause of cancer-associated mortality among US women with survival disparities seen across race, ethnicity, and socioeconomic status, even after accounting for histology, stage, treatment, and other clinical factors. Neighborhood context can play an important role in ovarian cancer survival, and, to the extent to which minority racial and ethnic groups and populations of lower socioeconomic status are more likely to be segregated into neighborhoods with lower quality social, built, and physical environment, these contextual factors may be a critical component of ovarian cancer survival disparities. Understanding factors associated with ovarian cancer outcome disparities will allow clinicians to identify patients at risk for worse outcomes and point to measures, such as social support programs or transportation aid, that can help to ameliorate such disparities. However, research on the impact of neighborhood contextual factors in ovarian cancer survival and in disparities in ovarian cancer survival is limited. This commentary focuses on the following neighborhood contextual domains: structural and institutional context, social context, physical context represented by environmental exposures, built environment, rurality, and healthcare access. The research conducted to date is presented and clinical implications and recommendations for future interventions and studies to address disparities in ovarian cancer outcomes are proposed.

Traffic-related Air Pollution and Lung Cancer Incidence: The California Multiethnic Cohort Study.

Rationale: Although the contribution of air pollution to lung cancer risk is well characterized, few studies have been conducted in racially, ethnically, and socioeconomically diverse populations. Objectives: To examine the association between traffic-related air pollution and risk of lung cancer in a racially, ethnically, and socioeconomically diverse cohort. Methods: Among 97,288 California participants of the Multiethnic Cohort Study, we used Cox proportional hazards regression to examine associations between time-varying traffic-related air pollutants (gaseous and particulate matter pollutants and regional benzene) and lung cancer risk (n = 2,796 cases; average follow-up = 17 yr), adjusting for demographics, lifetime smoking, occupation, neighborhood socioeconomic status (nSES), and lifestyle factors. Subgroup analyses were conducted for race, ethnicity, nSES, and other factors. Measurements and Main Results: Among all participants, lung cancer risk was positively associated with nitrogen oxide (hazard ratio [HR], 1.15 per 50 ppb; 95% confidence interval [CI], 0.99-1.33), nitrogen dioxide (HR, 1.12 per 20 ppb; 95% CI, 0.95-1.32), fine particulate matter with aerodynamic diameter <2.5 µm (HR, 1.20 per 10 µg/m3; 95% CI, 1.01-1.43), carbon monoxide (HR, 1.29 per 1,000 ppb; 95% CI, 0.99-1.67), and regional benzene (HR, 1.17 per 1 ppb; 95% CI, 1.02-1.34) exposures. These patterns of associations were driven by associations among African American and Latino American groups. There was no formal evidence for heterogeneity of effects by nSES (P heterogeneity > 0.21), although participants residing in low-SES neighborhoods had increased lung cancer risk associated with nitrogen oxides, and no association was observed among those in high-SES neighborhoods. Conclusions: These findings in a large multiethnic population reflect an association between lung cancer and the mixture of traffic-related air pollution and not a particular individual pollutant. They are consistent with the adverse effects of air pollution that have been described in less racially, ethnically, and socioeconomically diverse populations. Our results also suggest an increased risk of lung cancer among those residing in low-SES neighborhoods.

School racial segregation and long-term cardiovascular health among Black adults in the US: A quasi-experimental study.

BACKGROUND: Cardiovascular disease (CVD) disproportionately affects Black adults in the United States. This is increasingly acknowledged to be due to inequitable distribution of health-promoting resources. One potential contributor is inequities in educational opportunities, although it is unclear what aspects of education are most salient. School racial segregation may affect cardiovascular health by increasing stress, constraining socioeconomic opportunities, and altering health behaviors. We investigated the association between school segregation and Black adults' CVD risk. METHODS AND FINDINGS: We leveraged a natural experiment created by quasi-random (i.e., arbitrary) timing of local court decisions since 1991 that released school districts from court-ordered desegregation. We used the Panel Study of Income Dynamics (PSID) (1991 to 2017), linked with district-level school segregation measures and desegregation court order status. The sample included 1,053 Black participants who ever resided in school districts that were under a court desegregation order in 1991. The exposure was mean school segregation during observed schooling years. Outcomes included several adult CVD risk factors and outcomes. We fitted standard ordinary least squares (OLS) multivariable linear regression models, then conducted instrumental variables (IV) analysis, using the proportion of schooling years spent in districts that had been released from court-ordered desegregation as an instrument. We adjusted for individual- and district-level preexposure confounders, birth year, and state fixed effects. In standard linear models, school segregation was associated with a lower probability of good self-rated health (-0.05 percentage points per SD of the segregation index; 95% CI: -0.08, -0.03; p < 0.001) and a higher probability of binge drinking (0.04 percentage points; 95% CI: 0.002, 0.07; p = 0.04) and heart disease (0.01 percentage points; 95% CI: 0.002, 0.15; p = 0.007). IV analyses also found that school segregation was associated with a lower probability of good self-rated health (-0.09 percentage points; 95% CI: -0.17, -0.02, p = 0.02) and a higher probability of binge drinking (0.17 percentage points; 95% CI: 0.04, 0.30, p = 0.008). For IV estimates, only binge drinking was robust to adjustments for multiple hypothesis testing. Limitations included self-reported outcomes and potential residual confounding and exposure misclassification. CONCLUSIONS: School segregation exposure in childhood may have longstanding impacts on Black adults' cardiovascular health. Future research should replicate these analyses in larger samples and explore potential mechanisms. Given the recent rise in school segregation, this study has implications for policies and programs to address racial inequities in CVD.

Joint Associations of Race, Ethnicity, and Socioeconomic Status With Mortality in the Multiethnic Cohort Study.

Importance: Socioeconomic status may help delineate racial and ethnic inequities in mortality. Objective: To investigate the joint associations of race, ethnicity, and neighborhood and individual socioeconomic status with mortality. Design, Setting, and Participants: This prospective analysis used data from the Multiethnic Cohort Study. A population-based sample of participants recruited from California (mainly Los Angeles County) and Hawaii from 1993 to 1996 was followed up until 2013. African American, European American, Japanese American, Latino American, and Native Hawaiian men and women were included. Participants with baseline residential addresses that could not be geocoded or who were missing information on education or adjustment variables were excluded. Data analyses were conducted from January 2018 to December 2020. Exposures: Neighborhood socioeconomic status (nSES) was derived using US Census block group data on education, occupation, unemployment, household income, poverty, rent, and house values. Participants self-reported their highest education attainment. Five racial and ethnic groups, 2 states of residence, 2 nSES, and 2 education categories were combined to create a joint exposure variable. Low and high nSES were defined as quintiles 1 to 3 and 4 to 5, respectively. Low and high education levels were defined as high school or less and greater than high school graduate, respectively. Main Outcomes and Measures: All-cause, cardiovascular disease (CVD), cancer, and non-CVD and noncancer deaths were ascertained through 2013 via linkage to death certificates and the US National Death Index. Multivariable Cox proportional hazards regression analyses were conducted. Results: Among 182 912 participants (100 785 [55.1%] women and 82 127 [44.9%] men; mean [SD] age, 60.0 [8.9] years; 31 138 African American, 45 796 European American, 52 993 Japanese American, 39 844 Latino American, and 13 141 Native Hawaiian participants) with a mean (SD) follow-up of 17 (5) years, there were 63 799 total deaths, including 23 191 CVD deaths, 19 008 cancer deaths, and 21 235 non-CVD and noncancer deaths. The lowest all-cause mortality was found among 15 104 Japanese American participants in Hawaii with high nSES and high education (eg, 2870 all-cause deaths [19.0%]), and this population served as the reference group for all regression analyses. Native Hawaiian participants in Hawaii with low nSES and low education had the highest all-cause mortality HR (2.38; 95% CI, 2.21-2.57). African American and European American participants in California with low nSES and low education had the next highest all-cause mortality HRs (2.01; 95% CI, 1.91-2.11 and 1.98; 95% CI, 1.85-2.12, respectively). Latino American participants in California with low nSES had equivalent all-cause mortality HRs regardless of education level (high education: 1.57; 95% CI, 1.48-1.66; low education: 1.57; 95% CI, 1.50-1.65). Patterns for cause-specific mortality were similar to those for all-cause mortality. For example, Native Hawaiian participants in Hawaii with low nSES and low education had highest CVD mortality HR (2.92; 95% CI, 2.60-3.27) and cancer mortality HR (2.01; 95% CI, 1.77-2.29). Conclusions and Relevance: These results suggest that joint associations of nSES and education may further delineate racial and ethnic inequities in mortality and that future investigations of racial and ethnic inequities in mortality should consider differences by measures of socioeconomic status, especially for underserved populations.

School Racial Segregation and the Health of Black Children.

OBJECTIVES: Few researchers have evaluated whether school racial segregation, a key manifestation of structural racism, affects child health, despite its potential impacts on school quality, social networks, and stress from discrimination. We investigated whether school racial segregation affects Black children's health and health behaviors. METHODS: We estimated the association of school segregation with child health, leveraging a natural experiment in which school districts in recent years experienced increased school segregation. School segregation was operationalized as the Black-White dissimilarity index. We used ordinary least squares models as well as quasi-experimental instrumental variables analysis, which can reduce bias from unobserved confounders. Data from the Child Development Supplement of the Panel Study of Income Dynamics (1997-2014, n = 1248 Black children) were linked with district-level school segregation measures. Multivariable regressions were adjusted for individual-, neighborhood-, and district-level covariates. We also performed subgroup analyses by child sex and age. RESULTS: In instrumental variables models, a one standard deviation increase in school segregation was associated with increased behavioral problems (2.53 points on a 27-point scale; 95% CI, 0.26 to 4.80), probability of having ever drunk alcohol (0.23; 95% CI, 0.049 to 0.42), and drinking at least monthly (0.20; 95% CI, 0.053 to 0.35). School segregation was more strongly associated with drinking behaviors among girls. CONCLUSIONS: School segregation was associated with worse outcomes on several measures of well-being among Black children, which may contribute to health inequities across the life span. These results highlight the need to promote school racial integration and support Black youth attending segregated schools.

Contributions of Social Factors to Disparities in Prostate Cancer Risk Profiles among Black Men and Non-Hispanic White Men with Prostate Cancer in California.

BACKGROUND: Black men are more likely than Non-Hispanic White (NHW) men to be diagnosed with high-risk prostate cancer. We examined the extent to which social factors were associated with differences in prostate cancer risk profiles between Black men and NHW men [using a modification to the original D'Amico risk groups based on prostate specific antigen (PSA), Gleason score (GS), and TNM stage (stage)], based on individual and combined clinicopathologic characteristics. METHODS: We conducted a cross-sectional population-based study of 23,555 Black men and 146,889 NHW men diagnosed with prostate cancer in the California Cancer Registry from 2004 to 2017. We conducted multivariable logistic regression to examine the association of year of diagnosis, block group-level neighborhood socioeconomic status (nSES), marital status, and insurance type on differences in prostate cancer risk profiles between Black and NHW men. RESULTS: High PSA (>20 ng/mL), GS, stage, individually and combined prostate cancer risk profiles were more common among Black men versus NHW men. In fully adjusted models, relative to NHW men, we observed a persistent 67% increased odds of high PSA among Black men. nSES was the factor most strongly associated with racial disparity in high PSA, accounting for 25% of the difference. Marital status was the factor that was second most associated with a racial disparity. CONCLUSIONS: nSES was the factor most strongly associated with racial disparities in high PSA prostate cancer. IMPACT: The influence of nSES on racial disparities in PSA, GS, stage, and prostate cancer risk profiles warrants further consideration.

Association between Airport-Related Ultrafine Particles and Risk of Malignant Brain Cancer: A Multiethnic Cohort Study.

Ultrafine particles (UFP; diameter less than or equal to 100 nm) may reach the brain via systemic circulation or the olfactory tract and have been implicated in the risk of brain tumors. The effects of airport-related UFP on the risk of brain tumors are not known. Here we determined the association between airport-related UFP and risk of incident malignant brain cancer (n = 155) and meningioma (n = 420) diagnosed during 16.4 years of follow-up among 75,936 men and women residing in Los Angeles County from the Multiethnic Cohort study. UFP exposure from aircrafts was estimated for participants who lived within a 53 km × 43 km grid area around the Los Angeles International Airport (LAX) from date of cohort entry (1993-1996) through December 31, 2013. Cox proportional hazards models were used to estimate the effects of time-varying, airport-related UFP exposure on risk of malignant brain cancer and meningioma, adjusting for sex, race/ethnicity, education, and neighborhood socioeconomic status. Malignant brain cancer risk in all subjects combined increased 12% [95% confidence interval (CI), 0.98-1.27] per interquartile range (IQR) of airport-related UFP exposure (∼6,700 particles/cm3) for subjects with any address in the grid area surrounding the LAX airport. In race/ethnicity-stratified analyses, African Americans, the subgroup who had the highest exposure, showed a HR of 1.32 (95% CI, 1.07-1.64) for malignant brain cancer per IQR in UFP exposure. UFP exposure was not related to risk of meningioma overall or by race/ethnicity. These results support the hypothesis that airport-related UFP exposure may be a risk factor for malignant brain cancers. SIGNIFICANCE: Malignant brain cancer risk increases with airport-related UFP exposure, particularly among African Americans, suggesting UFP exposure may be a modifiable risk factor for malignant brain cancer.