Background: Research has linked neighborhood factors (e.g., air pollution, obesogenic environment) often associated with residential segregation to cancer disparities, including mortality. Limited research has explored these multilevel drivers of health, recognizing residential segregation as upstream of neighborhood social, built, and physical environment attributes. In this study, we describe the neighborhood data resource of the Pathways Study, a diverse cohort of women diagnosed with breast cancer. Methods: Using data from multiple sources, including the 2010 US Census, we appended census tract and block group-level measures that characterize the participants’ baseline neighborhoods. We examined distributions of neighborhood attributes by the Index of Concentration at the Extremes, a measure of racialized economic segregation, to demonstrate the relationships among these factors. Results: Twenty-eight percent of the participants resided in neighborhoods with the highest concentrations of high-income non-Hispanic White residents [i.e., most privileged neighborhoods; quintile (Q) 5] compared with only 9% who resided in neighborhoods with the highest concentrations of low-income residents from minoritized racial/ethnic groups (i.e., least privileged neighborhoods, Q1). Participants residing in less privileged neighborhoods had more exposure to detrimental neighborhood attributes, including a higher overall pollution burden, markers of physical disorder (e.g., graffiti and garbage), more barred windows, and a higher crime index. Conclusions: For a cohort of breast cancer survivors, residing in neighborhoods with less privilege shows evidence of adverse neighborhood attributes across domains of social, built, and physical environments. Impact: This neighborhood infrastructure is well positioned to assess interactions across the multilevel factors contributing to health disparities in women with breast cancer.

Evaporative coolers (ECs) introduce outdoor air pollutants indoors when operating. This study evaluates the potential of do-it-yourself (DIY) air filtration solutions for ECs to cost-effectively reduce the infiltration of ambient fine particulate matter (PM2.5) in homes with ECs using measurements in 48 homes in wildfire-affected agricultural communities in California. All homes received one portable air cleaner (PAC); 25 homes also received DIY filters (mostly MERV 13) attached to their ECs. PurpleAir monitors measured indoor and outdoor PM2.5 concentrations. PAC operation was monitored in all of the homes. EC usage was monitored in some homes and predicted using relative humidity dynamics in all homes. Conditional analyses between EC likely on and off conditions were used to evaluate the impacts of DIY EC filters on ambient PM2.5 infiltration, including during several wildfire-affected days. Median levels of ambient PM2.5 infiltration increased ∼36-42% in homes with only PAC interventions when ECs were likely operating compared to only ∼10-11% in homes with both PACs and DIY EC filters. Pre/postintervention comparisons in a subset of homes confirmed PM2.5 infiltration reductions. EC filter performance declined after extended use. Results suggest that short-term EC filter deployments are likely a cost-effective way to mitigate wildfire smoke infiltration inside these homes.

Although physical activity (PA) levels have been linked to decreased lung cancer mortality, the magnitude of associations and delineation of biological and behavioral risk factors are often inconsistent. Our study aims to address this gap by elucidating the associations of lung cancer survival while considering duration and intensity of prediagnosis PA levels. We evaluated lung cancer-specific survival among 1768 women diagnosed with lung cancer in the California Teachers Study (1995–2019). PA was assessed at baseline and included lifetime PA (cumulative activity from high school through age 54) and recent PA (activity during the 3 years prior to enrollment), each quantified separately for moderate and strenuous intensity. These measures capture both long-term duration and short-term duration of PA at different intensities before diagnosis. Multivariable Cox proportional hazards models using age as the time scale were used to estimate hazard ratios (HRs) and 95

SIC codes used to define food environment and recreational facilities variables

Lung cancer is a leading cause of cancer mortality for most ethnic groups of Asian American women, including Chinese, Korean, Japanese, and Vietnamese Americans, a striking pattern given the exceedingly low prevalence of smoking among Asian American women in the general population. Recent research demonstrates that among Asian American women with a lung cancer diagnosis, the vast majority of patients have never smoked, a rate as high as 80% among Chinese and Asian Indian American women. Despite declining rates in lung cancer overall in the United States, rates among Asian American women who have never smoked appear to be increasing. This commentary articulates extant knowledge, based on studies in Asia, of a range of risk factors, such as a family history of lung cancer; a history of lung diseases, including tuberculosis and chronic obstructive pulmonary disease; exposure to cooking fumes and second-hand smoke; and various putative risk factors. Unique mutational profiles at the tumor level, including a higher prevalence of EGFR variations among Asian populations, highlight the importance of tumor genomic testing of newly diagnosed patients. Additional research is essential, given the high burden of disease among Asian American women who have never smoked and the limited knowledge regarding contributing risk factors specific to Asian American women, because the risk factors identified in Asian people living in Asia may not apply.

ObjectiveTo evaluate the associations between brominated flame retardants (BFRs), including polybrominated diphenyl ethers (PBDEs), exposure and circulating immune markers in a subset of women from the California Teachers Study cohort.MethodsIn this cross-sectional study, serum from 813 female participants in the California Teachers Study collected in 2013–2016 were evaluated for 11 BFR congeners and 16 immune markers. Three BFR congeners [BDE153 [2,2′,4,4′,5,5′-Hexabromodiphenyl ether], BDE47 [2,2′,4,4′-Tetrabromodiphenyl ether], PBB153 [2,2′,4,4′,5,5′-Hexabromobiphenyl]] had median levels that were above the level of detection and were further evaluated for associations with circulating immune markers. Odds ratios (OR) and 95% confidence intervals (CI) were calculated by a logistic regression model where BFR congeners (in quartiles) were associated with immune markers (dichotomized as above and below the respective median), adjusted for age and total lipids. Sensitivity analyses were also conducted evaluating BFR congeners as a continuous exposure (per pg/ml).ResultsAll participants had at least one of the 11 measured BFR congeners detected in their serum. Increasing levels of BDE47 were associated with elevated levels of BAFF (B-cell activating factor; ORQuartile 4 = 1.67, 95% CI = 1.11–2.51), soluble CD27 (sCD27, cluster of differentiation 27; ORQuartile 4 = 1.69, 95% CI = 1.12–2.55) and IL6 (interleukin 6; ORQuartile 4 = 1.74, 95% CI = 1.13–2.66). Increasing levels of PBB153 were associated with elevated levels of CXCL13 (chemokine ligand 13; ORQuartile 4 = 1.55, 95% CI = 1.02–2.35) but inversely associated with sCD27 (ORQuartile 4 = 0.57, 95% CI = 0.38–0.87). Results from continuous models of BFR were largely consistent. No associations were observed between BDE153 and any of the immune markers assessed.ConclusionsTwo BFR congeners were statistically associated with altered levels of circulating immune markers involved in B cell activation pathways; replication and further evaluation of these novel associations are warranted. If confirmed, our results add to the current literature regarding possible immune mechanisms by which BFR exposures contribute to immune-related health endpoints and conditions where B cell activation is prominent, including autoimmune conditions.

Low-income families in dry regions, including in the Southwestern United States, frequently cool their homes with evaporative (“swamp”) coolers (ECs). While inexpensive and energy efficient compared to central air conditioners, ECs pull unfiltered outdoor air into the home, creating a health hazard to occupants when wildfire smoke and heat events coincide. A community-engaged research project to reduce wildfire smoke in homes was conducted in California’s San Joaquin Valley in homes of Spanish-speaking agricultural workers. A total of 88 study participants with ECs were asked about their level of satisfaction with their EC and their willingness to pay for air filtration. About 47% of participants reported dissatisfaction with their EC, with the most frequently reported reason being that it brings in dust and air pollution. Participants were highly satisfied with air cleaners and air filters that were offered to them free-of-charge. However, a willingness to pay analysis showed that air filtration solutions would not be adopted without significant subsidies; furthermore, air filtration would be an ongoing cost to participants due to the need to regularly replace filters. Short-term filtration solutions for EC users are feasible to implement and may reduce smoke exposure during wildfire events. Such solutions would need to be offered at low-or no-cost to reduce barriers to adoption. Longer term solutions include prioritizing homes with ECs in wildfire smoke exposed regions for replacement with air cooling technologies that provide clean air. Because ECs are disproportionately in low-income homes, addressing smoke intrusion through these devices is an environmental justice issue.

BACKGROUND:The American Cancer Society recommends physicians inform average-risk women about endometrial cancer risk on reaching menopause, but new diagnoses are rising fastest in women aged younger than 50 years. Educating these younger women about endometrial cancer risks requires knowledge of risk factors. However, endometrial cancer in young women is rare and challenging to study in single study populations. METHODS:We included 13 846 incident endometrial cancer patients (1639 aged younger than 50 years) and 30 569 matched control individuals from the Epidemiology of Endometrial Cancer Consortium. We used generalized linear models to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for 6 risk factors and endometrial cancer risk. We created a risk score to evaluate the combined associations and population attributable fractions for these factors. RESULTS:In younger and older women, we observed positive associations with body mass index and diabetes and inverse associations with age at menarche, oral contraceptive use, and parity. Current smoking was associated with reduced risk only in women aged 50 years and older (Phet < .01). Body mass index was the strongest risk factor (OR≥35 vs<25 kg/m2 = 5.57, 95% CI = 4.33 to 7.16, for ages younger than 50 years; OR≥35 vs<25 kg/m2 = 4.68, 95% CI = 4.30 to 5.09, for ages 50 years and older; Phet = .14). Possessing at least 4 risk factors was associated with approximately ninefold increased risk in women aged younger than 50 years and approximately fourfold increased risk in women aged 50 years and older (Phet < .01). Together, 59.1% of endometrial cancer in women aged younger than 50 years and 55.6% in women aged 50 years and older were attributable to these factors. CONCLUSIONS:Our data confirm younger and older women share common endometrial cancer risk factors. Early educational efforts centered on these factors may help mitigate the rising endometrial cancer burden in young women.

INTRODUCTION:Per- and polyfluoroalkyl substances (PFAS) are persistent environmental contaminants that have been linked to a number of health outcomes, including those related to immune dysfunction. However, there are limited numbers of epidemiological-based studies that directly examine the association between PFAS exposure and immune responses. METHODS:In this cross-sectional study nested in the California Teachers Study cohort, we measured nine PFAS analytes in serum. Of the 9 analytes, we further evaluated four (PFHxS [perfluorohexane sulfonate], PFNA [perfluorononanoic acid], PFOA [perfluorooctanoic acid], PFOS [perfluorooctanesulfonic acid]) that had detection levels of > 80 %, in relation to 16 systemic inflammatory/immune markers and corresponding immune pathways (Th1 [pro-inflammatory/macrophage activation], B-cell activation, and T-cell activation). Study participants (n = 722) were female, completed a questionnaire regarding various health measures and behaviors, and donated a blood sample between 2013-2016. The association between PFAS analytes and individual immune markers and pathways were evaluated by calculating odds ratios (OR) and 95 % confidence intervals (CI) in a logistic regression model. PFAS analytes were evaluated both as a dichotomous exposure (above or below the respective median) and as a continuous variable (per 1 unit increase [ng/mL]). RESULTS:The prevalence of detecting any PFAS analyte rose with increasing age, with the highest PFAS prevalence observed among those aged 75 + years and the lowest PFAS prevalence observed among those aged 40-49 years (study participant age range: 40-95 years). Significant associations with BAFF (B-cell activating factor) levels above the median were observed among participants with elevated (defined as above the median) levels of PFHxS (OR=1.53), PFOA (OR=1.43), and PFOS (OR=1.40). Similarly, there were statistically significant associations between elevated levels of PFHxS and TNFRII (tumor necrosis factor receptor 2) levels (OR=1.78) and IL2Rα (interleukin 2 receptor subunit alpha) levels (OR=1.48). We also observed significant inverse associations between elevated PFNA and sCD14 (soluble cluster of differentiation 14) (OR=0.73). No significant associations were observed between elevated PFNA and any immune marker. Evaluation of PFAS exposures as continuous exposures in association with dichotomized cytokines were generally consistent with the dichotomized associations. CONCLUSIONS:PFAS exposure was associated with altered levels of circulating inflammatory/immune markers; the associations were specific to PFAS analyte and immune marker. If validated, our results may suggest potential immune mechanisms underlying associations between the different PFAS analytes and adverse health outcomes.

AbstractHigher concentrations of ambient air pollutants, including PM2.5 and NO2, and other pollutants have been found near active oil and gas wells and may be associated with adverse COVID‐19 outcomes. We assessed whether residential exposure to nearby oil and gas production was associated with higher rates of the respiratory infection COVID‐19 and related mortality using a population‐based ecological study in California. Using gridded population estimates, we estimated area‐level exposure to annual average oil and gas production volume from active wells within 1 kilometer (km) of populated areas within census block groups from 2018 to 2020. We geocoded confirmed cases and associated deaths to assess block group case and mortality rates from COVID‐19 from February 2020 to January 2021. We fit hierarchical Poisson models with individual and area covariates (e.g., age, sex, socioeconomic disadvantage), and included time and other interactions to assess additional variation (e.g., testing, reporting rates). In the first 4 months of the study period (February–May 2020), block groups in the highest tertile of oil and gas production exposure had 34% higher case rates (IRR: 1.34 95% CI: 1.20, 1.49) and 55% higher mortality rates (MRR: 1.52 95%: CI: 1.14, 2.03) than those with no estimated production, after accounting for area‐level covariates. Over the entire study period, we observed moderately higher mortality rates in the highest group (MRR: 1.16 95%: CI: 1.01, 1.33) and null associations for case rates.

Per- and polyfluoroalkyl substances (PFAS) are persistent chemicals of increasing concern to human health. PFAS contamination in water systems has been linked to a variety of sources including hydrocarbon fire suppression activities, industrial and military land uses, agricultural applications of biosolids, and consumer products. To assess PFAS in California tap water, we collected 60 water samples from inside homes in four different geographic regions, both urban and rural. We selected mostly small water systems with known history of industrial chemical or pesticide contamination and that served socioeconomically disadvantaged communities. Thirty percent of the tap water samples (18) had a detection of at least one of the 32 targeted PFAS and most detections (89 %) occurred in heavily industrialized Southeast Los Angeles (SELA). The residents of SELA are predominately Latino and low-income. Concentrations of perfluorooctanoic acid (PFOA) and perfluorooctanesulfonic acid (PFOS) ranged from 6.8 to 13.6 ng/L and 9.4-17.8 ng/L, respectively in SELA and were higher than State (PFOA: 0.007 ng/L; PFOS: 1.0 ng/L) and national health-based goals (zero). To look for geographic patterns, we mapped potential sources of PFAS contamination, such as chrome plating facilities, airports, landfills, and refineries, located near the SELA water systems; consistent with the multiple potential sources in the area, no clear spatial associations were observed. The results indicate the importance of systematic testing of PFAS in tap water, continued development of PFAS regulatory standards and advisories for a greater number of compounds, improved drinking-water treatments to mitigate potential health threats to communities, especially in socioeconomically disadvantaged and industrialized areas.

Water is an increasingly precious resource in California as years of drought, climate change, pollution, as well as an expanding population have all stressed the state's drinking water supplies. Currently, there are increasing concerns about whether regulated and unregulated contaminants in drinking water are linked to a variety of human-health outcomes particularly in socially disadvantaged communities with a history of health risks. To begin to address this data gap by broadly assessing contaminant mixture exposures, the current study was designed to collect tapwater samples from communities in Gold Country, the San Francisco Bay Area, two regions of the Central Valley (Merced Fresno and Kern counties), and southeast Los Angeles for 251 organic chemicals and 32 inorganic constituents. Sampling prioritized low-income areas with suspected water quality challenges and elevated breast cancer rates. Results indicated that mixtures of regulated and unregulated contaminants were observed frequently in tapwater throughout the areas studied and the types and concentrations of detected contaminants varied by region, drinking-water source, and size of the public water system. Multiple exceedances of enforceable maximum contaminant level(s) (MCL), non-enforceable MCL goal(s) (MCLG), and other health advisories combined with frequent exceedances of benchmark-based hazard indices were also observed in samples collected in all five of the study regions. Given the current focus on improving water quality in socially disadvantaged communities, our study highlights the importance of assessing mixed-contaminant exposures in drinking water at the point of consumption to adequately address human-health concerns (e.g., breast cancer risk). Data from this pilot study provide a foundation for future studies across a greater number of communities in California to assess potential linkages between breast cancer rates and tapwater contaminants.

While links between certain chronotypes and poorer health outcomes have been well established in previous studies, few studies have examined the relationship between chronotype and cellular aging. Using data from the California Teachers Study (CTS), the present study evaluates the relationship between cellular aging and chronobiology through an analysis of leukocyte telomere length (LTL) and chronotype among 817 predominantly postmenopausal women with no history of cancer and occupations not associated with night-shift work. Unconditional logistic regression models were run to estimate odds ratios (ORs) for each chronotype category, adjusted for age, ethnicity, and smoking status. Analyses were then stratified by potential modifiers to assess whether results varied among specific subgroups within the sample. Women who reported being current evening types and evening types from teen years to now were significantly less likely to have short LTL compared to women who reported being current morning types or morning types from teen years to now (OR = 0.72; 95% CI = 0.53-0.98; OR = 0.57; 95% CI = 0.39-0.84). Our results suggest that women with no history of cancer who identify as evening chronotypes may undergo decreased cellular aging compared to women in the same population who identify as morning types. Further studies on populations of postmenopausal women are warranted.

The "Gold Country" region of California is impacted by legacy and active gold mines. Concomitantly, Gold Country has an increased rate of female breast cancer relative to the state average. Using community-based participatory research methods, 40 participants completed surveys and collected a total of 354 water, soil, home-grown foods, and dust samples from their homes, which we compared to state, federal, and international contamination standards for arsenic, cadmium, and lead. All soil samples exceeded U.S. EPA and California EPA soil standards for arsenic. When comparing other media to state, federal and international standards for arsenic, cadmium, and lead, 15 additional exceedances for indoor/outdoor dust, drinking water, and/or vegetable were documented. A probabilistic risk assessment was conducted to determine an adult female's exposure to arsenic, cadmium, and lead and estimated risk. Arsenic exposure, due largely to water (63.5 %) and homegrown food (33.3 %), presents carcinogenic risks in excess of the EPA recommended upper limit for contami-nated sites (1 x 10-4) in 12.5 % of scenarios, and exceeds a risk level of 1 x 10-6 in 98.0 % of cases. Cadmium exposure results mainly from homegrown food consumption (83.7 %), and lead exposure results from a broader range of sources. This research indicates that rural areas in Gold Country face environmental exposures different than in urban areas. Expo-sure to arsenic in the female population of Gold Country may be driven by consumption of home-grown foods and water, and exposure to cadmium is driven by home-grown food intake. Since mining sites are of concern internationally, this risk assessment process and associated findings are significant and can be used to inform and tailor public health interventions. The weight of the evidence suggests that the arsenic exposure identified in this study could contribute to increases in the cancer rate among those living in Gold Country, California.

Background Endometrial cancer risk stratification may help target interventions, screening, or prophylactic hysterectomy to mitigate the rising burden of this cancer. However, existing prediction models have been developed in select cohorts and have not considered genetic factors. Methods We developed endometrial cancer risk prediction models using data on postmenopausal White women aged 45-85 years from 19 case-control studies in the Epidemiology of Endometrial Cancer Consortium (E2C2). Relative risk estimates for predictors were combined with age-specific endometrial cancer incidence rates and estimates for the underlying risk factor distribution. We externally validated the models in 3 cohorts: Nurses' Health Study (NHS), NHS II, and the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial. Results Area under the receiver operating characteristic curves for the epidemiologic model ranged from 0.64 (95% confidence interval [CI] = 0.62 to 0.67) to 0.69 (95% CI = 0.66 to 0.72). Improvements in discrimination from the addition of genetic factors were modest (no change in area under the receiver operating characteristic curves in NHS; PLCO = 0.64 to 0.66). The epidemiologic model was well calibrated in NHS II (overall expected-to-observed ratio [E/O] = 1.09, 95% CI = 0.98 to 1.22) and PLCO (overall E/O = 1.04, 95% CI = 0.95 to 1.13) but poorly calibrated in NHS (overall E/O = 0.55, 95% CI = 0.51 to 0.59). Conclusions Using data from the largest, most heterogeneous study population to date (to our knowledge), prediction models based on epidemiologic factors alone successfully identified women at high risk of endometrial cancer. Genetic factors offered limited improvements in discrimination. Further work is needed to refine this tool for clinical or public health practice and expand these models to multiethnic populations.

PURPOSE:Poor sleep quality and evening chronotype were associated with increased risk of breast cancer in a previous retrospective study in the California Teachers Study (CTS). The present analysis examines these sleep factors prospectively in the same cohort of women.METHODS:From the CTS, we included 1,085 incident breast cancer cases and 38,470 cancer-free participants from 2012 through 2019. We calculated time at risk and used Cox proportional hazards regression models to estimate the hazard ratios (HRs) and control for risk factors such as age, race, body mass index, family history of breast cancer, and reproductive history. The sleep factors examined were quality, latency, duration, disturbance, and sleep medication use, based on a shortened version of the Pittsburgh Sleep Quality Index, as well as chronotype (preference for morning or evening activity). This analysis was limited to women who were post-menopausal at the time they answered these sleep-related questions.RESULTS:Measures of sleep quality did not appear to be associated with subsequent breast cancer risk. The HR for evening chronotypes compared to morning chronotypes was somewhat elevated (HR 1.19, 95% CI 1.04, 1.36).CONCLUSION:While the measures of sleep quality and duration were not associated with post-menopausal breast cancer risk in this prospective analysis, the modestly elevated risk observed for evening chronotypes was consistent with the prior retrospective analysis.

Background Some hormonally active cancers have low survival rates, but a large proportion of their incidence remains unexplained. Endocrine disrupting chemicals may affect hormone pathways in the pathology of these cancers. Objective To evaluate cross-sectional associations between per- and polyfluoroalkyl substances (PFAS), phenols, and parabens and self-reported previous cancer diagnoses in the National Health and Nutrition Examination Survey (NHANES). Methods We extracted concentrations of 7 PFAS and 12 phenols/parabens and self-reported diagnoses of melanoma and cancers of the thyroid, breast, ovary, uterus, and prostate in men and women (≥20 years). Associations between previous cancer diagnoses and an interquartile range increase in exposure biomarkers were evaluated using logistic regression models adjusted for key covariates. We conceptualized race as social construct proxy of structural social factors and examined associations in non-Hispanic Black, Mexican American, and other Hispanic participants separately compared to White participants. Results Previous melanoma in women was associated with higher PFDE (OR:2.07, 95% CI: 1.25, 3.43), PFNA (OR:1.72, 95% CI: 1.09, 2.73), PFUA (OR:1.76, 95% CI: 1.07, 2.89), BP3 (OR: 1.81, 95% CI: 1.10, 2.96), DCP25 (OR: 2.41, 95% CI: 1.22, 4.76), and DCP24 (OR: 1.85, 95% CI: 1.05, 3.26). Previous ovarian cancer was associated with higher DCP25 (OR: 2.80, 95% CI: 1.08, 7.27), BPA (OR: 1.93, 95% CI: 1.11, 3.35) and BP3 (OR: 1.76, 95% CI: 1.00, 3.09). Previous uterine cancer was associated with increased PFNA (OR: 1.55, 95% CI: 1.03, 2.34), while higher ethyl paraben was inversely associated (OR: 0.31, 95% CI: 0.12, 0.85). Various PFAS were associated with previous ovarian and uterine cancers in White women, while MPAH or BPF was associated with previous breast cancer among non-White women. Impact Statement Biomarkers across all exposure categories (phenols, parabens, and per- and poly- fluoroalkyl substances) were cross-sectionally associated with increased odds of previous melanoma diagnoses in women, and increased odds of previous ovarian cancer was associated with several phenols and parabens. Some associations differed by racial group, which is particularly impactful given the established racial disparities in distributions of exposure to these chemicals. This is the first epidemiological study to investigate exposure to phenols in relation to previous cancer diagnoses, and the first NHANES study to explore racial/ethnic disparities in associations between environmental phenol, paraben, and PFAS exposures and historical cancer diagnosis.

Supplemental Table 1. Neighborhood Characteristics for Pathways Participants by Race/Ethnicity/Nativity (n=4,354)

After the devastating wildfire that destroyed most of the town of Paradise, California in 2018, volatile organic compounds were found in water distribution pipes. Approximately 11 months after the fire, we collected tap water samples from 136 homes that were still standing and tested for over 100 chemicals. Each participant received a customized report showing the laboratory findings from their sample. Our goal was to communicate individual water results and chemical information rapidly in a way that was understandable, scientifically accurate, and useful to participants. On the basis of this process, we developed a framework to illustrate considerations and priorities that draw from best practices of previous environmental results return research and crisis communication, while also addressing challenges specific to the disaster context. We also conducted a follow-up survey on participants’ perceptions of the results return process. In general, participants found the results return communications to be understandable, and they felt less worried about their drinking water quality after receiving the information. Over one-third of the participants reported taking some kind of action around their water usage habits after receiving their results. Communication with participants is a critical element of environmental disaster research, and it is important to have a strategy to communicate results that achieves the goals of timeliness, clarity, and scientific accuracy, ultimately empowering people toward actions that can reduce exposure.

Previous studies have reported associations between air pollution and COVID-19 morbidity and mortality, but most have limited their exposure assessment to a large area, have not used individual-level variables, nor studied infections. We examined 3.1 million SARS-CoV-2 infections and 49,691 COVID-19 deaths that occurred in California from February 2020 to February 2021 to evaluate risks associated with long-term neighborhood concentrations of particulate matter less than 2.5 μm in diameter (PM2.5). We obtained individual address data on SARS-CoV-2 infections and COVID-19 deaths and assigned 2000-2018 1km-1km gridded PM2.5 surfaces to census block groups. We included individual covariate data on age and sex, and census block data on race/ethnicity, air basin, Area Deprivation Index, and relevant comorbidities. Our analyses were based on generalized linear mixed models utilizing a Poisson distribution. Those living in the highest quintile of long-term PM2.5 exposure had risks of SARS-CoV-2 infections 20% higher and risks of COVID-19 mortality 51% higher, compared to those living in the lowest quintile of long-term PM2.5 exposure. Those living in the areas of highest long-term PM2.5 exposure were more likely to be Hispanic and more vulnerable, based on the Area Deprivation Index. The increased risks for SARS-CoV-2 Infections and COVID-19 mortality associated with highest long-term PM2.5 concentrations at the neighborhood-level in California were consistent with a growing body of literature from studies worldwide, and further highlight the importance of reducing levels of air pollution to protect public health.