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The article presents a study on past and future federal drinking water testing for Tribal and non-Tribal Nations public water systems in the U.S. Topics discussed include the methods used in the study, factors that limit the implementation of per- and polyfluoroalkyl substance testing, and recommendations to provide resources and support for the inclusion of more Tribal public water system in systematic research.

Objectives. To assess the US incarcerated population's risk of exposure to per- and polyfluoroalkyl substances (PFASs). Methods. We assessed how many of the 6118 US carceral facilities were located in the same hydrologic unit code watershed boundaries as known or likely locations of PFAS contamination. We conducted geospatial analyses on data aggregated from Environmental Protection Agency databases and a PFAS site tracker in 2022 to model the hydrologically feasible known and presumptive PFAS contamination sites for nearly 2 million incarcerated people. Results. Findings indicate that 5% (∼310) of US carceral facilities have at least 1 known source of PFAS contamination in the same watershed boundary and that it is at a higher elevation than the facility; also 47% (∼2285) have at least 1 presumptive source. A minimum of 990 000 people are incarcerated in these facilities, including at least 12 800 juveniles. Exposure risks faced by incarcerated youths are disproportionately underassessed. Conclusions. The long-term impacts from potential exposures to PFAS are preventable and exacerbate health inequities among incarcerated populations. Widespread public attention to PFASs can be parlayed into broader environmental monitoring for imprisoned people. (Am J Public Health. 2024;114(5):501–510. https://doi.org/10.2105/AJPH.2024.307571) [ABSTRACT FROM AUTHOR]

Introduction: The American Heart Association's Life's Simple 7 includes seven metrics of ideal cardiovascular health to target for cardiovascular disease prevention. This study determined the relationship between Life's Simple 7 and incident peripheral artery disease in a biracial cohort of middle- and older-aged adults.Methods: This analysis included 12,865 participants from the Atherosclerosis Risk in Communities study recruited between 1987 and 1989 (mean age=54years, 55% women, 25% black) and free of peripheral artery disease or other cardiovascular disease at baseline. Overall, Life's Simple 7 score was calculated as the sum of the Life's Simple 7 component scores (two points if ideal, one point if intermediate, and zero if poor) and classified as inadequate (zero to four), average (five to nine), or optimal (ten to 14) cardiovascular health and linked to incident peripheral artery disease identified by hospital discharge diagnosis and leg revascularization. Analysis was conducted in 2017.Results: A total of 434 incident peripheral artery disease cases occurred over a median follow-up of 24.4years. Compared with the inadequate category (n=1,008), participants in the average (n=8,395) and optimal (n=3,462) categories each had a substantially lower risk of developing peripheral artery disease in a Cox proportional hazards model adjusted for potential confounders (hazard ratio=0.36, 95% CI=0.28, 0.46 for average, and hazard ratio=0.09, 95% CI=0.06, 0.15 for optimal). In a similar model, a one-point higher Life's Simple 7 score was associated with a 25% lower risk of incident peripheral artery disease (hazard ratio=0.75, 95% CI=0.72, 0.79).Conclusions: Better cardiovascular health, as defined by higher Life's Simple 7 score, is associated with a substantially lower risk of peripheral artery disease. [ABSTRACT FROM AUTHOR]

Background: Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease of motor neurons that results in progressive weakness and death from respiratory failure, commonly within about 3 years. Previous studies have shown association of a locus on chromosome 9p with ALS and linkage with ALS-frontotemporal dementia. We aimed to test whether this genomic region is also associated with ALS in an independent set of UK samples, and to identify risk factors associated with ALS in a further genome-wide association study that combined data from the independent analysis with those from other countries.Methods: We collected samples from patients with sporadic ALS from 20 UK hospitals and obtained UK control samples from the control groups of the Depression Case Control study, the Bipolar Affective Case Control Study, and the British 1958 birth cohort DNA collection. Genotyping of DNA in this independent analysis was done with Illumina HumanHap550 BeadChips. We then undertook a joint genome-wide analysis that combined data from the independent set with published data from the UK, USA, Netherlands, Ireland, Italy, France, Sweden, and Belgium. The threshold for significance was p=0·05 in the independent analysis, because we were interested in replicating a small number of previously reported associations, whereas the Bonferroni-corrected threshold for significance in the joint analysis was p=2·20×10(-7)Findings: After quality control, samples were available from 599 patients and 4144 control individuals in the independent set. In this analysis, two single nucleotide polymorphisms in a locus on chromosome 9p21.2 were associated with ALS: rs3849942 (p=2·22×10(-6); odds ratio [OR] 1·39, 95% CI 1·21-1·59) and rs2814707 (p=3·32×10(-6); 1·38, 1·20-1·58). In the joint analysis, which included samples from 4312 patients with ALS and 8425 control individuals, rs3849942 (p=4·64×10(-10); OR 1·22, 95% CI 1·15-1·30) and rs2814707 (p=4·72×10(-10); 1·22, 1·15-1·30) were associated with ALS.Interpretation: We have found strong evidence of a genetic association of two single nucleotide polymorphisms on chromosome 9 with sporadic ALS, in line with findings from previous independent GWAS of ALS and linkage studies of ALS-frontotemporal dementia. Our findings together with these earlier findings suggest that genetic variation at this locus on chromosome 9 causes sporadic ALS and familial ALS-frontotemporal dementia. Resequencing studies and then functional analysis should be done to identify the defective gene. [ABSTRACT FROM AUTHOR]