Policing and the punitive politics of local homelessness policy

Advocates and researchers agree that solutions to homelessness must address the root causes. Communities need to increase access to quality, affordable permanent housing and provide the necessary social and medical services to support unhoused people remaining stably housed. Yet, local governments may not always follow these evidence-based housing policy programs, instead pursuing punitive policing or the criminalization of homelessness. Such policies do not end homelessness and may actually promote cycles of homelessness. This policy brief investigates the involvement of the police in responses to homelessness in cities across the country. The authors amass a wide array of data, including a novel survey of mayors and details of Homeless Outreach Teams from the nation’s 100 largest cities. They find that the police are highly influential in city homelessness policymaking and are frequently involved in implementing homelessness policy.Community Solution

Early Life Exposure to Aflatoxin B1 in Rats: Alterations in Lipids, Hormones, and DNA Methylation among the Offspring

Aflatoxins are toxic compounds produced by molds of the Aspergillus species that contaminate food primarily in tropical countries. The most toxic aflatoxin, aflatoxin B1 (AFB1), is a major cause of hepatocellular carcinoma (HCC) in these countries. In sub-Saharan Africa, aflatoxin contamination is common, and perinatal AFB1 exposure has been linked to the early onset of HCC. Epigenetic programming, including changes to DNA methylation, is one mechanism by which early life exposures can lead to adult disease. This study aims to elucidate whether perinatal AFB1 exposure alters markers of offspring health including weight, lipid, and hormone profiles as well as epigenetic regulation that may later influence cancer risk. Pregnant rats were exposed to two doses of AFB1 (low 0.5 and high 5 mg/kg) before conception, throughout pregnancy, and while weaning and compared to an unexposed group. Offspring from each group were followed to 3 weeks or 3 months of age, and their blood and liver samples were collected. Body weights and lipids were assessed at 3 weeks and 3 months while reproductive, gonadotropic, and thyroid hormones were assessed at 3 months. Prenatal AFB1 (high dose) exposure resulted in significant 16.3%, 31.6%, and 7.5% decreases in weight of the offspring at birth, 3 weeks, and 3 months, respectively. Both doses of exposure altered lipid and hormone profiles. Pyrosequencing was used to quantify percent DNA methylation at tumor suppressor gene Tp53 and growth-regulator H19 in DNA from liver and blood. Results were compared between the control and AFB1 exposure groups in 3-week liver samples and 3-week and 3-month blood samples. Relative to controls, Tp53 DNA methylation in both low- and high-dose exposed rats was significantly decreased in liver samples and increased in the blood (p < 0.05 in linear mixed models). H19 methylation was higher in the liver from low- and high-exposed rats and decreased in 3-month blood samples from the high exposure group (p < 0.05). Further research is warranted to determine whether such hormone, lipid, and epigenetic alterations from AFB1 exposure early in life play a role in the development of early-onset HCC

Per- and polyfluoroalkyl substances, epigenetic age and DNA methylation: a cross-sectional study of firefighters

Background: Per- and polyfluoroalkyl substances (PFASs) are persistent chemicals that firefighters encounter. Epigenetic modifications, including DNA methylation, could serve as PFASs toxicity biomarkers. Methods: With a sample size of 197 firefighters, we quantified the serum concentrations of nine PFASs, blood leukocyte DNA methylation and epigenetic age indicators via the EPIC array. We examined the associations between PFASs with epigenetic age, site- and region-specific DNA methylation, adjusting for confounders. Results: Perfluorohexane sulfonate, perfluorooctanoate (PFOA) and the sum of branched isomers of perfluorooctane sulfonate (Sm-PFOS) were associated with accelerated epigenetic age. Branched PFOA, linear PFOS, perfluorononanoate, perfluorodecanoate and perfluoroundecanoate were associated with differentially methylated loci and regions. Conclusion: PFASs concentrations are associated with accelerated epigenetic age and locus-specific DNA methylation. The implications for PFASs toxicity merit further investigation. Lay abstract Per- and poly-fluoroalkyl substances (PFASs) are a group of toxic chemicals that populations around the world are widely exposed to through contaminated water and consumer products. Firefighters can also be exposed to PFASs from occupational practices. Epigenetic modifications, including DNA methylation, regulate gene expression. It can be modified by environmental exposures such as PFASs, which contribute to the development of diseases including cancer. We measured the concentrations of nine PFASs in samples from firefighters and profiled DNA methylation across the genome. Three PFASs were linked with accelerated epigenetic age, a marker associated with many diseases. Four PFASs were associated with altered DNA methylation levels at specific genes. These results may indicate how PFASs are harmful to health and merit further exploration