We aimed to evaluate the types and concentrations of trace elements in tears of individuals living in urban and rural environments using particle induced X-ray emission (PIXE) and the possible association with exposure to air pollution and suggest a novel method for tear-based biomonitoring studies. This cross-sectional pilot study comprised 42 healthy subjects, 28 living in a rural area and 14 in an industrial city. Tears were collected with Schirmer paper and characterized by PIXE. Trace element concentrations from both eyes were averaged together with environmental pollution data. Main outcome measures were between-group differences in types and concentrations of trace elements in tears and comparison to environmental data. The rural group included 12/28 men, mean age 45.2 ± 14.8 years. The urban group consisted of 11/14 men of mean age 27 ± 5.9 years. Six rural and all urban were active smokers. Air pollution data showed more toxic elements in the rural environment. On PIXE analysis, chlorine, sodium, and potassium were found in similar concentrations in all samples. Normalizing to chlorine yielded higher values of aluminum, iron, copper, and titanium in the rural group; aluminum was found only in the rural group. The higher levels of certain trace elements in the rural group may, in part, be a consequence of exposure to specific environmental conditions. No direct association was found with air pollution data. PIXE is useful to analyze trace elements in tears, which might serve as a marker for individual exposure to environmental pollutants in biomonitoring studies.

Cobalt toxicity is difficult to detect and therefore often underdiagnosed. The aim of this study was to explore the pathophysiology of cobalt-induced oxidative stress in the brain and its impact on structure and function. Thirty-five wild-type C57B16 mice received intraperitoneal cobalt chloride injections: a single high dose with evaluations at 24, 48, and 72 h (n = 5, each) or daily low doses for 28 (n = 5) or 56 days (n = 15). A part of the 56-day group also received minocycline (n = 5), while 10 mice served as controls. Behavioral changes were evaluated, and cobalt levels in tissues were measured with particle-induced X-ray emission. Brain sections underwent magnetic resonance imaging (MRI), electron microscopy, and histological, immunohistochemical, and molecular analyses. High-dose cobalt caused transient illness, whereas chronic daily low-dose administration led to long-term elevations in cobalt levels accompanied by brain inflammation. Significant neurodegeneration was evidenced by demyelination, increased blood–brain barrier permeability, and mitochondrial dysfunction. Treated mice exhibited extended latency periods in the Morris water maze test and heightened anxiety in the open field test. Minocycline partially mitigated brain injury. The observed signs of neurodegeneration were dose- and time-dependent. The neurotoxicity after acute exposure was reversible, but the neurological and functional changes following chronic cobalt administration were not.