Aug 2026· International Journal of Epidemiology· Vol 55· 0 citations
Medicine
Abstract
Background: Under the top-secret Manhattan Project, improperly stored radioactive byproducts from the processing of uranium contaminated Coldwater Creek in north St. Louis County, Missouri. We used the original 1958 Baby Tooth Survey (BTS) linked with the National Death Index (NDI) to investigate whether childhood residential proximity to the creek, as a proxy for radiation exposure, was associated with mortality. Methods: There were 43,876 eligible participants from the BTS (those outside Greater St. Louis and/or had incomplete covariates were excluded). In December 2023, the NDI was searched for BTS participants who have died. We estimated the hazard ratio (HR) and 95% confidence intervals between distance to Coldwater Creek (per 10km) and mortality (all-cause, cancer, and cardiovascular disease) adjusting for sex, birth year and census tract-level socioeconomic indicators. Results: Living closer to Coldwater Creek was associated with a higher rate of all-cause mortality (HR: 1.05; 95% CI: 1.01-1.09; p=0.01). There was suggestive evidence of an increased rate for cancer mortality: any cancer (HR: 1.06; 95% CI: 1.00-1.14; p=0.06), solid cancer (HR: 1.07, 95% CI: 1.00-1.16; p=0.06) and radiosensitive cancer (HR: 1.10; 95% CI: 1.00-1.21; p=0.05). There was no association with non-radiosensitive cancer and cardiovascular mortality. Conclusions: Our study provides new data that suggests living near Coldwater Creek in childhood was positively associated with the rate of all-cause mortality, and to a lesser extent cancer mortality, but not cardiovascular disease mortality. However, these findings should be interpreted cautiously given the lack of data on internal radiation exposure and individual socioeconomic status.
BACKGROUND
The C8 Science Panel previously conducted studies of perfluorooctanoic acid (PFOA) exposure in Ohio Valley residents, finding probable links with kidney and testicular cancers, raised cholesterol, ulcerative colitis, thyroid disease, and pre-eclampsia. Findings were largely based on a cohort of 32,254 persons with high PFOA exposure followed through 2011 for disease incidence. We have now followed this cohort through 2021 for mortality.
METHODS
Deaths were ascertained via the National Death Index (NDI). We extended cumulative PFOA serum estimates from 2011 until 2021. We used internal comparisons via Cox regression models to analyze cause-specific mortality for 22 causes of death in relation to natural log transformed cumulative PFOA exposure (continuous and in quartiles) with a variety of lags, controlling for confounders. We also considered multiple cause of death.
RESULTS
There were 5709 deaths in the cohort through 2021. We found a positive significant trend (p < 0.05) in underlying cause of death analyses between the log cumulative serum level and brain cancer [HR 1.25 (1.05, 1.50)] and a suggestive but non-statistically significant association with bladder cancer [HR 1.17 (0.98, 1.39). . In stratified analysis, pancreatic cancer showed a positive significant trend among older participants (>72 years) [HR 1.23 (1.05, 1.43)]. No other causes showed marked positive trends, except for stroke among workers (13 % of total cohort).
CONCLUSION
PFOA exposure was significantly associated with mortality from brain cancer, and pancreatic cancer among older subjects. Pancreatic cancer has been associated with PFOA in animal studies, with equivocal evidence in other cohort studies. There was some suggestion of an increase of bladder cancer Caution is warranted due to multiple comparisons.
You-Ran Tan, Jonathan N. Hofmann, Vaughn Barry et al.· Environment International· 0 citations
Air pollution is the leading environmental risk factor in the U.S. for premature morbidity and mortality and disproportionately impacts marginalized populations. Although the causal link between air pollution and lung cancer is well established, its impact on breast cancer is less understood. Therefore, in this study, we examined the association between traffic-related air pollution (NO
2
) and particulate matter (PM
2.5
) with the development of breast cancer-specific subtypes among non-Hispanic Black (NHB) and non-Hispanic White (NHW) women in Georgia.
Using the Georgia Cancer Registry, we identified women with a first primary breast cancer diagnosis 2010–2017 and geocoded their address at diagnosis to the census tract level. Daily PM
2.5
and NO
2
concentrations modeled on a 1-km grid (SEDAC) were aggregated to census tracts and averaged to annual means; women were assigned the annual mean concentration lagged 5 years prior to diagnosis based on tract of residence at diagnosis. We used logistic regression to compute case-only odds ratios (ORs) and 95% confidence intervals (CIs) associating air pollutant concentrations to a diagnosis of triple negative breast cancer (TNBC) compared with other breast cancer subtypes, overall and in strata of race/ethnicity and rurality.
We identified 13,634 NHB and 29,508 NHW women diagnosed with first primary breast cancer between 2010 and 2017 in Georgia. After adjustment for age at diagnosis, race, rurality, and neighborhood poverty, a 5 µg/m
3
increase in PM
2.5
was associated an increase in the odds of TNBC (OR = 1.11, 95%CI 1.02, 1.21) among all breast cancer patients, with no evidence of effect modification by race or rurality. In the fully adjusted model, a 5-ppb increase in NO
2
was associated with a decrease in the odds of ER-negative breast cancer (OR = 0.98, 95%CI 0.96, 0.99) and these effect estimates were consistent within racial groups and by rurality.
Our results indicate etiologic heterogeneity by breast cancer subtype, with PM
2.5
associated with higher odds of TNBC and NO
2
weakly associated with ER-positive disease; however, these associations were consistent across race and rurality, with no evidence of effect modification.
Leah Moubadder, L. J. Collin, M. Maliniak et al.· Breast Cancer Research· 0 citations
Background: In urban areas, transportation and industry-related combustion processes release large quantities of outdoor ultrafine particles (UFPs; <0.1 µm). Due to their small size, UFPs can cross biological barriers, including the placenta, and reach vital organs. Exposure during critical windows of development may increase the risk of adverse health outcomes in children, including cancer. Methods: We conducted a cohort study of over 965,000 children born in Canada between 1999 and 2020 whose birthing parent resided in Montreal or Toronto during pregnancy. Vital status and cancer incidence were obtained from the Canadian Vital Statistics Databases and the Canadian Cancer Registry. High-resolution estimates of outdoor UFP number concentrations and UFP size (i.e., mean particle diameter for a given UFP number concentration) were assigned to children’s six-digit residential postal codes from annual tax records. We estimated hazard ratios (HRs) between outdoor UFP number concentrations and childhood cancer using Cox proportional hazards models, adjusting for UFP size, sociodemographic factors, and co-pollutants. Results: Children were followed from 0 to 14 years old for a mean of 9.1 years. In total, 1,625 children were diagnosed with cancer. For each 10,000 particles/cm3 increase in prenatal UFP exposure, we observed positive associations with acute lymphoblastic leukemia (ALL) (HR: 1.12; 95% confidence interval [CI]: 0.94, 1.34) and neuroblastoma (HR: 1.15; 95% CI: 0.85, 1.57), although estimates were imprecise and included the null. Consistent associations were also observed for these outcomes across different exposure windows and multiple sensitivity analyses. In contrast, null associations were observed for central nervous system tumors, and an inverse association was observed for lymphoma. Conclusion: Overall, our findings varied depending on the cancer diagnostic group evaluated. Positive associations observed between outdoor UFPs and ALL and neuroblastoma warrant further research.
E. Batisse, M. Lloyd, É. Lavigne et al.· Environmental Epidemiology· 0 citations
Fallout containing radioactive byproducts of plutonium production at the Hanford atomic weapons facility near Richland, WA secretly blanketed downwind civilian populations, called “Downwinders”, throughout the Inland Northwest. Research into health impacts has been hindered by the decades-long delay between these releases which began with the site’s start-up in November 1944 and declassification of Hanford operational records disclosing these releases in 1986. Downwinders observed and prior analyses suggested an apparent excess in fetal and neonatal deaths during the 1940s and 1950s. Analysis of radiation released by Hanford, the possible cause of these deaths, has been hampered by data access and time. The few existing studies relied on uncertain, estimated exposure doses from the heavily criticized government-sponsored Hanford Environmental Dose Reconstruction project. Women and children, lower-socioeconomic status, non-white, and Indigenous communities are commonly overburdened by exposures to radioactive contamination and lack of subsequent care and study. This commentary highlights the unanswered questions surrounding pregnancy outcomes impacted by exposures to airborne and river-borne radiation from Hanford, documents the process and barriers to addressing these questions, and calls for increased accessibility of information, especially for impacted communities.
Olivia M. Vaz, Trisha T. Pritikin, Elizabeth S. McClure· Inquiry : a journal of medic...· 0 citations
The authors' findings suggest distinct patterns of joint associations for birth defects, providing further evidence of the effects of pesticide mixtures, and future research should prioritize individual-level studies to validate and extend these ecological associations.
Jabeen Taiba, Cheryl L. Beseler, Muhammad Zahid et al.· Environmental Research: Heal...· 0 citations
The results highlight fine-scale pollution variability not captured by regulatory monitors and underscore the need for spatially resolved assessments to guide public health interventions.
Abdulrahman N Alobireed, S. Totoni, L. Wigington et al.· Environmental science and po...· 0 citations
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