Carbon monoxide (CO), có độ độc cao, không mùi, không màu, không vị, dễ cháy khí được sử dụng như là một hóa chất khử trong các hoạt động luyện kim, trong tổng hợp hữu cơ của các loại sản phẩm dầu mỏ, và trong sản xuất của carbonyls kim loại. Độc tính của nó nằm trong khả năng của mình để kết hợp với hemoglobin trong máu để tạo thành carboxyhemoglobin, phá vỡ sự vận chuyển oxy và phân phối khắp cơ thể. Bà mẹ hút thuốc lá có thể tạo thành nguồn phổ biến nhất (thai nhi) tiếp. | Carbon Monoxide Chemical name CO Alternate names Carbonic oxide exhaust gas illuminating gas flue gas CAS 630-08-0 SMILES O C- O C INTRODUCTION Carbon monoxide CO is a highly poisonous odorless colorless tasteless flammable gas used as a reducing chemical in metallurgical operations in organic synthesis of petroleum-type products and in the manufacture of metal carbonyls. Its toxicity resides in its ability to combine with the hemoglobin in the blood to form carboxyhemoglobin which disrupts oxygen transport and delivery throughout the body. Maternal smoking probably constitutes the most common source of fetal exposure to high concentrations of CO measurements exceed 50 000 ppm in some cases Robinson and Forbes 1975 . This source of the chemical will not be discussed in this section. Rather exposures discussed here are in the context of human environmental atmospheric exposures. The threshold limit value TLV adopted for CO for the human is 25 ppm time weighted average its toxic activity is via anoxia to the cardiovascular central nervous and reproductive systems ACGIH 2005 . We will discuss the latter two systems here as developmental neurotoxicity is the primary manifestation of the effects of CO in the human see below . DEVELOPMENTAL TOXICOLOGY Animals Carbon monoxide inhalation has not proven to be a consistent teratogen in laboratory animals. As a multitude of studies in a variety of species have been conducted a tabulation of developmental effects by exposure level and response is provided in Table 1. The characteristic responses indicate that developmental toxicity in the form of embryolethality growth retardation and postnatal functional impairment is commonly induced in laboratory animals from CO exposures and rarely malformation is induced only in the rat and guinea pig. Humans In the human the pattern of toxicity recorded was mainly confined to the central nervous system and representative historical references over the interval 1929 to contemporary times
