The adrenal glands secrete higher amounts of DHEA-S during adrenarche (a stage of puberty), and this leads to an increase in sebum production. In a sebum-rich skin environment, the naturally occurring and largely commensal skin bacterium C. acnes readily grows and can cause inflammation within and around the follicle due to activation of the innate immune system. C. acnes triggers skin inflammation in acne by increasing the production of several pro-inflammatory chemical signals (such as IL-1α, IL-8, TNF-α, and LTB4); IL-1α is essential to comedo formation.C. acnes ability to bind and activate a class of immune system receptors known as toll-like receptors (TLRs), especially TLR2 and TLR4, is a core mechanism of acne-related skin inflammation. Activation of TLR2 and TLR4 by C. acnes leads to increased secretion of IL-1α, IL-8, and TNF-α. The release of these inflammatory signals attracts various immune cells to the hair follicle, including neutrophils, macrophages, and Th1 cells. IL-1α stimulates increased skin cell activity and reproduction, which, in turn, fuels comedo development. Furthermore, sebaceous gland cells produce more antimicrobial peptides, such as HBD1 and HBD2, in response to the binding of TLR2 and TLR4.C. acnes also provokes skin inflammation by altering the fatty composition of oily sebum. Oxidation of the lipid squalene by C. acnes is of particular importance. Squalene oxidation activates NF-κB (a protein complex) and consequently increases IL-1α levels. Additionally, squalene oxidation increases 5-lipoxygenase enzyme activity, which catalyzes the conversion of arachidonic acid to leukotriene B4 (LTB4).
Noise exposure is the cause of approximately half of all cases of hearing loss, causing some degree of problems in 5% of the population globally. The majority of hearing loss is not due to age, but due to noise exposure. Various governmental, industry and standards organizations set noise standards. Many people are unaware of the presence of environmental sound at damaging levels, or of the level at which sound becomes harmful. Common sources of damaging noise levels include car stereos, childrens toys, motor vehicles, crowds, lawn and maintenance equipment, power tools, gun use, musical instruments, and even hair dryers. Noise damage is cumulative; all sources of damage must be considered to assess risk. In the US, 12.5% of children aged 6–19 years have permanent hearing damage from excessive noise exposure. The World Health Organization estimates that half of those between 12 and 35 are at risk from using personal audio devices that are too loud. Hearing loss in adolescents may be caused by loud noise from toys, music by headphones, and concerts or events.Hearing loss can be inherited. Around 75–80% of all these cases are inherited by recessive genes, 20–25% are inherited by dominant genes, 1–2% are inherited by X-linked patterns, and fewer than 1% are inherited by mitochondrial inheritance. Syndromic deafness occurs when there are other signs or medical problems aside from deafness in an individual, such as Usher syndrome, Stickler syndrome, Waardenburg syndrome, Alports syndrome, and neurofibromatosis type 2.