Abstract
Exposure to loud noise is a major environmental threat to public health. Loud noise exposure, apart from affecting the inner ear, is deleterious for cardiovascular, endocrine and nervous systems and it is associated with neuropsychiatric disorders. In this study we investigated DNA, neurotransmitters and immune-histochemical alterations induced by exposure to loud noise in three major brain areas (cerebellum, hippocampus, striatum) of Wistar rats. Rats were exposed to loud noise (100 dBA) for 12 h. The effects of noise on DNA integrity in all three brain areas were evaluated by using Comet assay. In parallel studies, brain monoamine levels and morphology of nigrostriatal pathways, hippocampus and cerebellum were analyzed at different time intervals (24 h and 7 days) after noise exposure. Loud noise produced a sudden increase in DNA damage in all the brain areas under investigation. Monoamine levels detected at 7 days following exposure were differently affected depending on the specific brain area. Namely, striatal but not hippocampal dopamine (DA) significantly decreased, whereas hippocampal and cerebellar noradrenaline (NA) was significantly reduced. This is in line with pathological findings within striatum and hippocampus consisting of a decrease in striatal tyrosine hydroxylase (TH) combined with increased Bax and glial fibrillary acidic protein (GFAP). Loud noise exposure lasting 12 h causes immediate DNA, and long-lasting neurotransmitter and immune-histochemical alterations within specific brain areas of the rat. These alterations may suggest an anatomical and functional link to explain the neurobiology of diseases which prevail in human subjects exposed to environmental noise.
Highlights
Noise pollution has become a severe issue in public health
It has been estimated that the burden of disease from environmental noise leads to 61,000 disability-adjusted life-years lost (DALYs) due to hypertension-related ischemic heart disease and related heart disorders; 45,000 DALYs derive from cognitive impairment which occurs even in children and young people. 903,000 DALYs are related to sleep disorders for people living in towns owing more than 50,000 inhabitants. 22,000 DALYs are due to tinnitus
This study demonstrates that loud noise exposure produces a damage to different brain areas, as assessed by genetic, biochemical and morphological analysis
Summary
Noise pollution has become a severe issue in public health. During daily life, people are exposed to hazardous noise levels produced by a variety of sources such as work environment, urban traffic, household appliances, loud music, etc. (Kawecka-Jaszcz, 1991; Lang et al, 1992). People are exposed to hazardous noise levels produced by a variety of sources such as work environment, urban traffic, household appliances, loud music, etc. The World Health Organization estimated that roughly 20% of Europeans are exposed to loud noise generated by urban traffic exceeding 65 dBA, which represents the safety threshold (Berglund et al, 1999). 40% is exposed to noise levels between 55 dBA and 65 dBA (below the safety threshold), which when reiterated over time, might still contribute to the onset of a number of disorders (Berglund et al, 1999). The DALYs attributed to noise in Western European countries were more than those attributed to lead (100–900), ozone (30–140) and dioxin (200–600) (WHO (World Health Organization), 2011)
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