Does tobacco cause aging?

Alireza FIROOZ and his team sought to compare the biophysical properties of the skin in smokers and non-smokers. To do this, smokers and non-smokers underwent tests to measure skin elasticity parameters, the thickness of the epidermis and dermis, as well as density. The depth of the right nasolabial folds was also measured.

Results : Elasticity was lower in smokers at the forehead level. The thickness of the dermis was higher in smokers on the cheek (2361.54 μm versus 2105.95 μm). The density of the epidermis was lower in smokers on the forehead (101.16 versus 124.13), and that of the dermis was lower in smokers on the arm (58.7 versus 72.65). The volume and surface area of the nasolabial folds were higher in smokers, but only the difference in surface area was significant.

We can therefore say that tobacco causes premature skin aging, through the appearance of wrinkles and fine lines, and a dull complexion. We often refer to this as the "smoker's face" with deep wrinkles, prominent bone contours, and a grayish skin discoloration, due to the slowing down of the renewal of the epidermal cells which then accumulate.

What are the biological mechanisms involved?

Changes in the macromolecular metabolism of the dermis are a major factor in skin aging. Molecular alterations in the dermis include the decrease in collagen synthesis, the induction of matrix metalloproteinases (MMP), and the abnormal accumulation of elastic fibers and proteoglycans. It has been shown that smokers have fewer collagen and elastin fibers in the dermis; this finding may justify the low density of the dermis in smokers. Indeed, the biosynthesis of new collagen and its precursors (procollagen I and III) is significantly reduced by tobacco smoke in cultured skin fibroblasts.

The accumulation of elastosis material, or the lysis of elastic tissue, is accompanied by the degradation of matrix proteins, mediated by MMPs in skin aging. MMPs constitute a family of enzymes responsible for the degradation of extracellular matrix components, such as collagen, elastin fibers, and various proteoglycans. The mRNA expression of MMP-1 and MMP-3, members of the MMP family associated with the extracellular membrane, has been induced in cultured skin fibroblasts treated with cigarette smoke. These results confirm the idea that MMPs are the main mediators of skin aging.

These MMPs are activated by the reactive oxygen species (ROS). These can be contained in tobacco smoke in the form of nitrogen species, or can be produced in response to tobacco smoke during oxidative stress. The tar phase of the cigarette contains several relatively stable free radicals, such as a quinone/hydroquinone complex (Q/QH2). This Q/QH2 polymer can function as an active redox system by reducing molecular oxygen in the lungs of smokers to produce O2.- radicals, which, in turn, reduce molecular oxygen in the lungs of smokers to produce O2.- radicals. They then activate the MMPs, which contribute to skin aging. These species can also amplify these effects themselves by oxidizing tissues and degrading dermal fibers.