Pulmonary infection, lung cancer
Acetone, methylethylketone, n-propanol
Diabetes mellitus (uncontrolled)
Rooth and Ostenson (1966)
Liver (hepatic) cirrhosis
Musty, fresh cadaver (“fetor hepaticus”)
Dimethyl sulfide, ketones
Van den Velde et al. (2008)
Kidney (renal) failure, uremia
Ammoniac, urine like
Ammonia, dimethylamine, trimethylamine
Simenhoff et al. (1977)
Fish like (“fish odor syndrome”)
Preti et al. (1992)
O’Reilly and Motley (1977)
Besouw et al. (2007)
Allyl methyl sulfide
Suarez et al. (1999)
Methyl propyl sulfide
Trimethyl pyridine dimethyl pyrazine
Bazemore et al. (2006)
More commonly, exogenous sources such as food substances, smoking, or medications may also play a part in breath odor formation (Table 7.1). These various sources may contribute odor components either directly from the upper respiratory tract or indirectly through the blood via alveolar air. The latter is also referred to as “blood borne halitosis” (Tangerman and Winkel 2010). In this case, the odor component is absorbed through the blood stream and released through the alveoli into the lung air. As such, these breath odors will be present in both the mouth and nasal exhalations.
Breath odors may originate from neoplasm and infections of the lower respiratory tract such as bronchogenic carcinoma, bronchiectasis, and anaerobic pulmonary infection (Gordon et al. 1985; Lorber 1975; Preti et al. 1988). The chemical analysis of breath samples from patients with lung cancer has shown elevated levels of acetone, methylethylketone, and n-propanol (Gordon et al. 1985). Alternatively, putrid smell might appear following a secondary bacterial infection of the tumor. Although putrid breath odor typically appears relatively late in the course of an anaerobic lung infection, following other symptoms such as fever, cough, and chest pains, it has been reported that in some cases it can serve as an early sign of the disease (Lorber 1975).
The “odor of decaying apples” on the breath of patients with uncontrolled diabetes mellitus was first recorded in the late eighteenth century (Crofford et al. 1977). In uncontrolled patients, this disease, which is termed “hunger in the midst of plenty,” causes an increase in lipid metabolism that results in the ketonic breath. This results from the formation of acetone, acetoacetate, and b-hydroxybutyrate, which are transferred from the blood to the alveolar air and exhaled through the breath (Rooth and Ostenson 1966). Furthermore, diabetes also affects oral health and may aggravate oral diseases and conditions (e.g., gingivitis, periodontitis, and decrease in saliva flow) that contribute to oral malodor production (Ship 2003).
Liver cirrhosis may give rise to a characteristic breath odor known as Fetor hepaticus. This is a sweet, musty, or slightly fecal smell on the breath which sometimes resembles the smell of a fresh cadaver. The impaired liver function decreases the metabolism of various malodorous compounds such as dimethyl sulfide and other ketones causing their increased blood levels and appearance on the breath (Van den Velde et al. 2008).
“Uremic breath” is a typical breath odor of patients with end-stage chronic renal failure. This type of breath odor has been described as “ammoniacal”, “urine-like”, and “fetid” odor and was attributed mainly to amine compounds such as dimethylamine and trimethylamine (Simenhoff et al. 1977