Long-term exposure to PM2.5-bound metals and female breast cancer incidence in New Mexico, USA

Long-term PM2.5 exposure and leukemia risk from childhood to early adulthood: A nationwide longitudinal cohort study with time-varying exposure analysis.

Long-term exposure to fine particulate matter (PM2.5) has been suggested as an environmental risk factor for childhood leukemia. This study examined the association between time-varying PM2.5 exposure and leukemia incidence in a nationwide cohort of Korean children and adolescents. We used data from the National Health Insurance Service-National Sample Cohort (2002-2020), including beneficiaries aged 0-18 years at enrollment who were followed until leukemia onset, death, or study end. Leukemia onset was defined as the first hospital visit with a primary diagnostic code from the 10th revision of the International Classification of Diseases. Annual PM2.5 concentrations were assigned to all 226 inland districts in South Korea using mean predictions from a machine learning-based ensemble model. Cox regression models with time-varying exposures and confounders were applied. Two-pollutant models incorporating NO2 and O3 were conducted as sensitivity analyses. Among 384,606 individuals aged 0-18 at enrollment, 272 developed leukemia during follow-up, including 83 who were diagnosed after the age of 18 years. The cohort's average annual PM2.5 concentration was 29.6 μg/m3 (standard deviation: 3.1). Each 5 μg/m3 increase in annual PM2.5 was associated with a hazard ratio of 1.40 (95% confidence interval: 1.04-1.90) for leukemia. The effect estimate remained comparable when follow-up was censored at age 18 years, suggesting that the findings were not materially influenced by the inclusion of diagnoses occurring after age 18. Long-term PM2.5 exposure was associated with increased leukemia incidence in this national cohort. These findings underscore the importance of reducing air pollution to protect the health of children and adolescents.

Chemical composition of fine particulate matter and all-cause mortality of older lung cancer patients.

Ambient fine particulate matter (PM2.5) is a proven human lung carcinogen associated with lung cancer incidence. However, the relative toxicity of the various chemical components of PM2.5 and their joint association with all-cause mortality following lung cancer diagnosis remain unclear. We conducted a cohort study of 528,127 adults aged ≥65 years with lung cancer diagnosed between 2000-2019, derived from the SEER-Medicare database. Patients were followed annually from diagnosis until death, loss to follow-up, or end of the study in 2019. Two-year moving average exposures to 15 PM2.5 chemical components were estimated using high-resolution spatiotemporal models and linked to each patient based on residential ZIP code in each year. We used generalized weighted quantile sum regression with random holdouts to estimate both the joint association of PM2.5 component mixtures with all-cause mortality and the relative contribution of each component, adjusted for demographics, histological type, stage, first-course treatments, comorbidities, and neighborhood-level covariates. We found that joint exposure to PM2.5 component mixtures was associated with increased mortality, with relative risk of 1.011 (95% confidence interval [CI]: 1.010, 1.013) per decile increase in all components. Although differences in contributions were modest, silicon, nitrate, vanadium, zinc, and iron appeared to be more influential contributors, suggesting that controlling related sources, such as road dust, traffic emissions, fossil fuel combustion, and heavy fuel oil combustion, may obtain greater potential benefits. Exploratory subgroup analyses suggested that the joint association may be stronger among patients with non-small cell lung cancer, those with later-stage disease, and female patients.

Occupational exposure to metals and prostate cancer: CAPLIFE study.

Few studies have explored the association between occupational metal exposure and prostate cancer (PCa), without considering combined effects and tumor characteristics. The aim is to analyze the potential individual and joint exposure to occupational metals on PCa risk, considering tumor aggressiveness and stage. CAPLIFE is a case-control study that included 464 cases and 428 controls. Lifetime occupational exposure to chromium (Cr), nickel (Ni), iron (Fe), and lead (Pb) was estimated using the Spanish job-exposure matrix (MatEmESp). Metal exposure was defined as: i) ever vs. never exposure; ii) lifetime cumulative exposure (prevalence*intensity*duration); and iii) duration (years), both categorized into tertiles (T) based on controls. Multivariable logistic regression and Quantile g-Computation models assessed individual and joint effects, stratified by International Society of Urological Pathology (ISUP) grade and tumor stage [localized and locally advanced (cT3/cT4 or N1) or metastatic (M1) tumors]. No association was observed between individual metal exposure and overall PCa, nor when stratified by ISUP grade. For locally advanced or metastatic tumors, higher odds were observed for Cr, Ni, and Fe. Specifically, the strongest associations were observed for Ni [exposure, aORevervsnever= 1.99 (95%CI 1.02-3.89), lifetime cumulative exposure, aORT3vsnever= 3.53 (95%CI 1.34-9.30), and duration, aOR T3vsnever= 3.58 (95%CI 1.37-9.37)]. Metal mixture exposure was also associated with locally advanced or metastatic tumors, aOR= 1.41 (95%CI 1.04-1.91), with Ni showing the only positive weight. In conclusion, no association was found for overall PCa, nor with the ISUP grade. However, exposure to Cr, Ni, and Fe, as well as joint metal exposure, was linked to higher odds of locally advanced or metastatic PCa. Although these results should be interpreted with caution as occupational exposure was estimated using a job-exposure matrix, they may, if confirmed, support preventive strategies to reduce occupational metal exposure.

Water Arsenic Levels and Breast Cancer Risk in a United States-Wide Prospective Cohort.

In the U.S., drinking water is an important source of exposure to inorganic arsenic, an established human carcinogen. Chronic exposure to low levels of inorganic arsenic (≤10 μg/L) has been linked to bladder and kidney cancers; however, the association with other cancers remains inconsistent. We investigated the association between arsenic from private wells and community water systems and breast cancer incidence in a large U.S.-wide prospective cohort. Among 33,864 Sister Study participants residing in states with available arsenic data and reporting eligible water source types at enrollment (2003-2009), geocoded residential addresses were linked to county-level water arsenic concentrations. For community water system (CWS) users (n=27,290), addresses were linked to county-level water arsenic concentrations using the EPA National Contaminant Occurrence database (2006-2008). For well water users (n =6,574), addresses were linked to county-level modeled probabilities that arsenic levels in private well water exceeded 10 μg/L. Cox proportional hazards regression was used to estimate adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the association between water arsenic and incident breast cancer, with subgroup analyses by tumor subtypes and menopausal status. Over 13.2 years (mean) of follow-up, 3,309 breast cancer cases (invasive and ductal carcinoma in situ) were diagnosed. We observed non-monotonic but elevated associations between increasing levels of water arsenic and invasive breast cancer risk (CWS HRQ5vsQ1=1.11, 95%CI 0.98-1.27, P-trend=0.16; Well HRQ5vsQ1=1.11, 95%CI 0.84-1.47, P-trend=0.88). When stratified by hormone receptor status and menopausal status, the associations did not meaningfully differ between subgroups. In a nationwide prospective cohort, we observed a suggestive positive association between relatively higher water arsenic levels and breast cancer incidence; however, the non-monotonic trends and exposure assessment limitations warrant further investigation. These results suggest that levels of arsenic in water in the U.S. may contribute to breast cancer risk.

Association between long-term exposure to environmental coarse particulate matter and the prevalence of thyroid disorders: a cross-sectional study in China.

Exposure to Particulate Matter (PM) During Pregnancy and Non-Hodgkin Lymphomas in Children

Background/Objectives: Lymphomas are the third most common pediatric malignancy, with non-Hodgkin lymphoma (NHL) comprising around 7% of childhood cancers. Environmental exposures have been linked to its etiology. Particulate matter (PM) prenatal exposure is increasingly scrutinized for potential effects on early-life carcinogenesis. We investigated whether exposure during pregnancy to PM2.5 and PM10 was associated with childhood NHL incidence. Methods: A population-based case–control study was conducted in Spain (2009–2016), including 3,682,038 children < 15 years. Incident NHL cases (n = 289) were identified through the Spanish Childhood Tumor Registry. Prenatal PM2.5 and PM10 exposures were estimated using a random forest model. Logistic regression estimated odds ratios (ORs) and 95% confidence intervals (CIs). Exposures were modeled continuously and categorically by tertiles (low, medium, or high exposure) to assess nonlinearity; trimester-specific analyses were also explored. Results: In the analysis with the continuous exposure, higher prenatal PM2.5 was associated with increased odds of NHL, and PM10 showed smaller associations. With categorical variables, medium and high-level exposure to PM2.5 showed an association with higher NHL incidence, especially in the third trimester. High-level exposure to PM10 during the first and second trimesters was linked to a higher NHL incidence in children under five years. Conclusions: Maternal PM2.5 and PM10 exposure during pregnancy could be associated with childhood NHL incidence, with stronger associations among children diagnosed before age 5. These findings warrant replication and mechanistic investigation.