The skin, our body’s largest organ, acts as a primary defense. While it forms a robust barrier, some toxic substances can bypass it, even when the skin appears undamaged. Understanding this penetration is important for comprehending their potential effects. This article explores how chemicals cross the skin barrier, detailing the specific pathways and influencing factors.
The Skin’s Natural Barrier
The skin’s protective function resides in its outermost layer, the epidermis, specifically the stratum corneum. This layer is often described using a “bricks and mortar” analogy. Flattened, dead skin cells (corneocytes) act as “bricks,” providing structural strength. These are embedded in a lipid-rich matrix, the “mortar,” which holds them together and forms a continuous, semi-permeable barrier.
This arrangement prevents excessive water loss and blocks the entry of many foreign substances, including toxins. The stratum corneum’s composition (keratin in corneocytes, lipids in matrix) makes it a strong obstacle. Its integrity is important for maintaining skin health and protecting deeper tissues.
Main Routes of Entry
Despite the skin’s barrier, toxic substances can find pathways to penetrate. Three primary routes allow chemicals to traverse the stratum corneum: the intercellular, transcellular, and appendageal routes. These pathways dictate how a substance moves past the skin’s initial defenses.
The intercellular route involves substances moving between corneocytes, through the lipid matrix. This pathway is often most significant for smaller, lipid-soluble molecules, as they diffuse readily through the fatty “mortar.” Though tortuous, this lipid-filled space presents resistance, yet remains a common entry point.
The transcellular route requires substances to pass directly through the corneocytes. This means a chemical must cross both the lipid membranes and the aqueous, protein-rich interior (keratin). While direct, substances encounter alternating lipid and aqueous environments, making it challenging for many compounds to traverse.
The appendageal route utilizes natural skin openings like hair follicles and sweat glands. These offer direct conduits to deeper layers, bypassing much of the stratum corneum. However, this route accounts for a smaller fraction of absorption because these openings represent only 0.1% to 1.0% of the total skin surface area.
Factors Affecting Absorption
Several factors influence how easily a toxic substance permeates the skin. The substance’s intrinsic properties affect its ability to cross the barrier. Smaller molecules (below 500 Daltons) penetrate more readily than larger ones. Lipid-soluble (lipophilic) substances are absorbed more efficiently through the lipid-rich stratum corneum. The substance’s concentration on the skin surface and its pH also impact absorption rate.
Skin condition also affects permeability. Hydration levels alter the stratum corneum’s structure; well-hydrated skin may be more permeable. Skin temperature can increase absorption, as higher temperatures enhance diffusion and blood flow. The anatomical site of exposure also matters, as skin thickness and composition vary across body regions, leading to differing absorption rates.
The duration of contact between the substance and the skin is another important determinant. Longer exposure times lead to greater absorption of the chemical into the body. This highlights the importance of minimizing contact time with potentially harmful substances to reduce the risk of significant uptake.
Beyond the Skin: Systemic Entry
Once a toxic substance navigates through the stratum corneum and viable epidermis, it continues deeper into the body. It reaches the dermal layer, beneath the epidermis, which is rich in blood and lymphatic vessels. Upon reaching these vessels, the substance can be absorbed into the bloodstream or lymphatic system. From there, it enters systemic circulation, distributing throughout the body. This widespread distribution allows the absorbed chemical to potentially affect internal organs, completing its route from external exposure to internal presence.