Pyridine might also have minor neurotoxic, genotoxic, and clastogenic effects. Exposure to pyridine would normally lead to its inhalation and absorption in the lungs and gastrointestinal tract, where it either remains unchanged or is metabolized. The major products of pyridine metabolism are "N"-methylpyridiniumhydroxide, which are formed by "N"-methyltransferases (e.g., pyridine "N"-methyltransferase), as well as pyridine "N"-oxide, and 2-, 3-, and 4-hydroxypyridine, which are generated by the action of monooxygenase. In humans, pyridine is metabolized only into "N"-methylpyridiniumhydroxide. Pyridine is readily degraded by bacteria to ammonia and carbon dioxide. The unsubstituted pyridine ring degrades more rapidly than picoline, lutidine, chloropyridine, or aminopyridines, and a number of pyridine degraders have been shown to overproduce riboflavin in the presence of pyridine. Ionizable "N"-heterocyclic compounds, including pyridine, interact with environmental surfaces (such as soils and sediments) via multiple pH-dependent mechanisms, including partitioning to soil organic matter, cation exchange, and surface complexation. Such adsorption to surfaces reduces bioavailability of pyridines for microbial degraders and other organisms, thus slowing degradation rates and reducing ecotoxicity.