On average, exposures at 100 ppm or greater is dangerous to human health. In the United States, the OSHA limits long-term workplace exposure levels to less than 50 ppm averaged over an 8-hour period; in addition, employees are to be removed from any confined space if an upper limit ("ceiling") of 100 ppm is reached. +Effects of<unk><unk>  in relation to the concentration in parts per million in the air: Concentration Symptoms 35 ppm (0.0035%), (0.035‰) Headache and dizziness within six to eight hours of constant exposure 100 ppm (0.01%), (0.1‰) Slight headache in two to three hours 200 ppm (0.02%), (0.2‰) Slight headache within two to three hours; loss of judgment 400 ppm (0.04%), (0.4‰) Frontal headache within one to two hours 800 ppm (0.08%), (0.8‰) Dizziness, nausea, and convulsions within 45 min; insensible within 2 hours 1,600 ppm (0.16%), (1.6‰) Headache, increased heart rate, dizziness, and nausea within 20 min; death in less than 2 hours 3,200 ppm (0.32%), (3.2‰) Headache, dizziness and nausea in five to ten minutes. Death within 30 minutes. 6,400 ppm (0.64%), (6.4‰) Headache and dizziness in one to two minutes. Convulsions, respiratory arrest, and death in less than 20 minutes. 12,800 ppm (1.28%), (12.8‰) Unconsciousness after 2–3 breaths. Death in less than three minutes. Acute poisoning CO toxicity symptoms The main manifestations of<unk>  develop in the organ systems most dependent on oxygen use, the central nervous system and the heart. The initial symptoms of acute<unk>  include headache, nausea, malaise, and fatigue. These symptoms are often mistaken for a virus such as influenza or other illnesses such as food poisoning or gastroenteritis. Headache is the most common symptom of acute<unk> ; it is often described as dull, frontal, and continuous. Increasing exposure produces cardiac abnormalities including fast heart rate, low blood pressure, and cardiac arrhythmia; central nervous system symptoms include delirium, hallucinations, dizziness, unsteady gait, confusion, seizures, central nervous system depression, unconsciousness, respiratory arrest, and death. Less common symptoms of acute<unk>  include myocardial ischemia, atrial fibrillation, pneumonia, pulmonary edema, high blood sugar, lactic acidosis, muscle necrosis, acute kidney failure, skin lesions, and visual and auditory problems.<unk><unk>  exposure may lead to a significantly shorter life span due to heart damage. One of the major concerns following acute<unk>  is the severe delayed neurological manifestations that may occur. Problems may include difficulty with higher intellectual functions, short-term memory loss, dementia, amnesia, psychosis, irritability, a strange gait, speech disturbances, Parkinson's disease-like syndromes, cortical blindness, and a depressed mood. Depression may occur in those who did not have pre-existing depression. These delayed neurological sequelae may occur in up to 50% of poisoned people after 2 to 40 days. It is difficult to predict who will develop delayed sequelae; however, advanced age, loss of consciousness while poisoned, and initial neurological abnormalities may increase the chance of developing delayed symptoms. Chronic poisoning Chronic exposure to relatively low levels of<unk><unk>  may cause persistent headaches, lightheadedness, depression, confusion, memory loss, nausea, hearing disorders and vomiting. It is unknown whether low-level chronic exposure may cause permanent neurological damage. Typically, upon removal from exposure to<unk><unk> , symptoms usually resolve themselves, unless there has been an episode of severe acute poisoning. However, one case noted permanent memory loss and learning problems after a three-year exposure to relatively low levels of<unk><unk>  from a faulty furnace. Chronic exposure may worsen cardiovascular symptoms in some people. Chronic<unk><unk>  exposure might increase the risk of developing atherosclerosis. Long-term exposures to<unk><unk>  present the greatest risk to persons with coronary heart disease and in females who are pregnant. In experimental animals,<unk><unk>  appears to worsen noise-induced hearing loss at noise exposure conditions that would have limited effects on hearing otherwise. In humans, hearing loss has been reported following<unk> . Unlike the findings in animal studies, noise exposure was not a necessary factor for the auditory problems to occur. Fatal poisoning One classic sign of<unk>  is more often seen in the dead rather than the living – people have been described as looking red-cheeked and healthy (see below). However, since this "cherry-red" appearance is more common in the dead, it is not considered a useful diagnostic sign in clinical medicine. In autopsy examinations, the appearance of<unk>  is notable because unembalmed dead persons are normally bluish and pale, whereas dead<unk><unk>  poisoned people may appear unusually lifelike in coloration. The colorant effect of<unk><unk>  in such postmortem circumstances is thus analogous to its use as a red colorant in the commercial meat-packing industry.
Carbon monoxide poisoning
Cyanide poisoning
Nitrogen dioxide poisoning
Upper respiratory tract infection
Chlorine gas poisoning
Alcoholic ketoacidosis
Salicylate poisoning
Theobromine poisoning