Global wealth disparities drive adherence to COVID-safe pathways in head and neck cancer surgery

Peer reviewe

Manganese exposure, parkinsonian signs, and quality of life in South African mine workers

BACKGROUND: Manganese neurotoxicity is associated with parkinsonism; the associated motor deficits can affect individuals’ quality of life (QoL). We investigated associations between manganese (Mn) exposure, parkinsonian signs, and QoL in Mn mine workers. METHODS: We assessed parkinsonian signs and QoL in 187 black South African Mn mine workers, using the Unified Parkinson Disease Rating Scale motor subsection 3 (UPDRS3), and the Parkinson Disease Questionnaire (PDQ-39), respectively. We estimated cumulative Mn exposure in mg Mn/m(3)-years using complete occupational histories and a job exposure matrix. We investigated the cross-sectional association between cumulative Mn exposure and UPDRS3 score, and the UPDRS3 score and PDQ-39, adjusting for age, using linear regression. RESULTS: Participants mean age was 41.8 years (range 21–67 years); 97.3% were male. Estimated mean cumulative Mn exposure at the time of examination was 5.4 mg Mn/m(3)-years, with a mean of 14.0 years working in a Mn mine. The mean UPDRS3 score was 10.1, and 25.7% of the workers had a UPDRS3 score ≥ 15. There was a U-shaped dose-response relation between cumulative Mn exposure and UPDRS3 score, with a positive association up to 15 mg Mn/m(3)-years of exposure and an inverse association thereafter. Greater UPDRS3 scores were associated with poorer self-reported QoL. CONCLUSION: In this cohort of employed Mn mine workers, parkinsonian signs were common, and were associated with both estimated cumulative Mn exposure and poorer quality of life

Air pollution and children: Neural and tight junction antibodies and combustion metals, the role of barrier breakdown and brain immunity in neurodegeneration

Millions of children are exposed to concentrations of air pollutants, including fine particulate matter (PM2.5), above safety standards. In the Mexico City Metropolitan Area (MCMA) megacity, children show an early brain imbalance in oxidative stress, inflammation, innate and adaptive immune response-associated genes, and blood-brain barrier breakdown. We investigated serum and cerebrospinal fluid (CSF) antibodies to neural and tight junction proteins and environmental pollutants in 139 children ages 11.91 ± 4.2 y with high versus low air pollution exposures. We also measured metals in serum and CSF. MCMA children showed significantly higher serum actin IgG, occludin/zonulin 1 IgA, IgG, myelin oligodendrocyte glycoprotein IgG and IgM (p < 0.01), myelin basic protein IgA and IgG, S-100 IgG and IgM, and cerebellar IgG (p < 0.001). Serum IgG antibodies to formaldehyde, benzene, and bisphenol A, and concentrations of Ni and Cd were significantly higher in exposed children (p < 0.001). CSF MBP antibodies and nickel concentrations were higher in MCMA children (p = 0.03). Air pollution exposure damages epithelial and endothelial barriers and is a robust trigger of tight junction and neural antibodies. Cryptic 'self' tight junction antigens can trigger an autoimmune response potentially contributing to the neuroinflammatory and Alzheimer and Parkinson's pathology hallmarks present in megacity children. The major factor determining the impact of neural antibodies is the integrity of the blood-brain barrier. Defining the air pollution linkage of the brain/immune system interactions and damage to physical and immunological barriers with short and long term neural detrimental effects to children's brains ought to be of pressing importance for public health