Azocarbonamide and Food – more environmental pollutants

Azodicarbonamide (AZA)  is a low molecular weight foaming agent used in plastics, rubbers, and as an oxidizer in flour to give it texture. The chemical is a condensed version of hydrazine and urea (H2N-OC-N=N-CO-NH2) which allows modification of other products by high expansion and self-dispersion of this chemical to create foaming.  In it’s use for food as a  dough conditioner, it has a volume/texture effect on the finished loaf, serving as a functional ingredient to improve the ‘quality’ of the bread.  Per the FDA, if the amount of ADA  is more than 45 ppm (.0045%) then the presence of ADA must be on the label. Other approved oxidizers include potassium bromate, calcium bromate, potassium iodate, calcium iodate and calcium peroxide. The  maximum use levels of these other oxidizers are  75 ppm based on flour. Also permitted are dehydro-L-ascorbic acid, added in the form of ascorbic acid at an unrestricted level. This is what is used in Europe to add quality to the dough.

Historically the use of oxidizers resulted from changes in the way wheat flour is shipped to factories. In the past, wheat flour would oxidize naturally over the long times spent in shipment to the factories, however, with more secure means of shipment (sealed bins, bulk tank trucks, and multiwall paper sacks) flour arrives at bakeries faster and ‘greener’ with less oxidization of the flour. Oxidized flour produces better quality breads. Holding bread for fermentation to oxidize in the bakeries is uneconomical and hence the use of oxidizer, such as ADA. The use of ADA shortens the required fermentation time and produces bread with a finer cell structure, which makes the crumb appear whiter. Bread made with ADA has a higher volume, finer grain, thinner cell walls and softer texture, and the dough has better handling characteristics. Concerning the exposure to ADA, it is more likely to occur in the factory workers using the ADA for oxidization. Likewise, as far as semicarbazide, one’s exposure is higher from glass jars with plastic lids

Azodicarbonamide, as a bleaching agent and improving agent, is a permitted food additive in certain countries and it’s presence can be determined by high-performance liquid chromatography. However, it partially degrades with the heat of processing to form trace amounts of semicarbazide, which shows carcinogenicity and also has been shown to cause tumors. It also is associated with cutaneous and pulmonary hypersensitivity.

Assessment of the Determination of Azodicarbonamide and Its Decomposition Product Semicarbazide: Investigation of Variation in Flour and Flour Products

Azodicarbonamide acts as an oxidizer in flour to condition the flour.

Its safety sheet can be found here:

Azodicarbonamide safety Card

Azodicarbonamide has had multiple uses, including as a ‘blowing agent’ in vinyl mats, where at high temperature, it breaks down to form bubbles. Carpet underlays and floor mats are made spongier by this bubble formation. Yoga mats, in particular, gained fame from containing this chemical. The Yoga Mat Chemical CNN

At one point, Azodicarbonamide (ADA) was being investigated to treat HIV virus: Phase I/II dose escalation and randomized withdrawal study with add-on azodicarbonamide in patients failing on current antiretroviral therapy In addition, ADA had synergy with cyclosporine to suppress T cell function: Azodicarbonamide as a new T cell immunosuppressant: synergy with cyclosporin A. Tassignon J, Vandevelde M, Goldman M – Clin. Immunol. – July 1, 2001; 100 (1); 24-30     Also noted in that ADA inhibits T cell responses:Azodicarbonamide inhibits T-cell responses in vitro and in vivo  and that it had some effect in HIV as well:Azodicarbonamide inhibits HIV-1 replication by targeting the nucleocapsid protein

Unfortunately, breakdown products of ADA are carcinogenic and there is an association of ADA with occupational asthma:Kim C, Cho J, Leem J, Ryu J, Lee H, Hong Y. Occupational asthma due to azodicarbonamide. Yonsei Med J. 2004; 45-2: 325-329.

Azodicarbonamide is readily converted to biurea, the only breakdown product identified, and it is likely that systemic exposure is principally to this derivative rather than to the parent compound.  Elimination of absorbed azodicarbonamide/biurea is rapid, occurring predominantly via the urine, and there is very little systemic retention of biurea. The chemical appears to be well absorbed by the inhalation and oral routes in rodents. From the WHO summary regarding ADA:

Evidence that azodicarbonamide can induce asthma in humans has been found from bronchial challenge studies with symptomatic individuals and from health evaluations of employees at workplaces where azodicarbonamide is manufactured or used. There are also indications that azodicarbonamide may induce skin sensitization. On the basis that azodicarbonamide is a human asthmagen and that the concentrations required to induce asthma in a non-sensitive individual or to provoke a response in a sensitive individual are unknown, it is concluded that there is a risk to human health under present occupational exposure conditions. The level of risk is uncertain; hence, exposure levels should be reduced as much as possible. The principal end use of azodicarbonamide is as a blowing agent in the rubber and plastics industries. It is used in the expansion of a wide range of polymers, including polyvinyl chloride, polyolefins, and natural and synthetic rubbers. The blowing action occurs when the azodicarbonamide decomposes on heating (process temperatures ~190–230 °C) to yield gases (nitrogen, carbon monoxide, carbon dioxide, and ammonia), solid residues, and sublimated substances. Decomposition accelerators, in the form of metal salts and oxides, may also be added to bring about decomposition at lower temperatures Azodicarbonamide has in the past been used in the United Kingdom and Eire (but not other European Union member states) as a flour improver in the bread-making industry, but this use is no longer permitted. Data have been identified that indicate ethyl carbamate formation in consumer products such as bread and beer following the addition of azodicarbonamideThe effects of long-term exposure to azodicarbonamide have not been well studied, and no conventional carcinogenicity studies are available. The only data come from l- and 2-year studies in which rats and dogs received diets containing various amounts of biurea. In the 1-year study, rats and dogs ate diets containing 5 or 10% biurea (Oser et al., 1965). One high-dose rat died, and body weight gain was slightly depressed in high-dose males. No other signs of toxicity were observed in rats at necropsy. Most dogs from both dose groups died. Necropsy revealed massive, multiple renal calculi, bladder calculi, and chronic pyelonephritis. Azodicarbonamide is mutagenic in vitro, inducing base-pair mutations in bacteria with and without metabolic activation (Pharmakon Research International, 1984a; Mortelmans et al., 1986; Hachiya, 1987)  In contrast, several standard in vitro assays in mammalian cell systems have yielded negative results A number of reports have been published of individual azodicarbonamide workers alleging asthma induced by exposure to azodicarbonamide. The strongest evidence comes from a study of two individuals (one atopic and one non-atopic) who worked at the same plastics factory for about 4 years (Malo et al., 1985; Pineau et al., 1985). Both wereintermittently exposed (1–2 weeks’ duration, 3–4 times per year) to azodicarbonamide at work. A few months after their first encounter with azodicarbonamide, both developed symptoms described as “eye/nose irritation” at work, followed a few hours later by nocturnal asthmatic symptoms. After a 1- month period free from exposure, both subjects underwent lung provocation studies. Baseline values for forced expiratory volume in 1 s (FEV1 ), forced vital capacity (FVC), and the concentration of histamine required to produce a 20% drop in FEV1 (PC20H) were obtained by spirometry. The link to the WHO paper is here:WHO statement regarding Azodicarbonamide

Occupational asthma caused by a plastics blowing agent, azodicarbonamide

Occupational Asthma due to Azodicarbonamide

PDF version Occupational asthma due to Azocarbonamide

A link to contact dermatitis due to ADA is found here: Azodicarbonamide and cutaneous sensitization

ADA is used widely – link to Natural News issue

Environmental Working Group release on products with ADA

Assessment of the determination of azodicarbonamide and its decomposition product semicarbazide: investigation of variation in flour and flour products. Ye J, Wang XH, Sang YX, Liu Q – J. Agric. Food Chem. – September 14, 2011; 59 (17); 9313-8 : Abstract is below: 

Azodicarbonamide, as a bleaching agent and improving agent, is a permitted food additive in certain countries and can be determined by high-performance liquid chromatography. However, it partially degrades with the heat of processing to form trace amounts of semicarbazide, which shows carcinogenicity and also has been shown to cause tumors. The concentration of semicarbazide in azodicarbonamide-treated flour was determined by isotope dilution ((13)C, (15)N(2)-semicarbazide) liquid chromatography electrospray tandem mass spectrometry (LC-MS/MS). The quantification was obtained utilizing the homologous internal standard. The limits of detection were 1 mg/kg for azodicarbonamide and 0.5 × 10(-3) mg/kg for semicarbazide. The rates of recovery were 82.3-103.1% for azodicarbonamide and 72.4-116.5% for semicarbazide. This study prepared four different types of flour products to investigate the variation of semicarbazide. The concentration of semicarbazide in all types of flour products is higher than that in flour, and the concentration of semicarbazide in outside of flour products is slightly higher than that in the inside. As the problem of food safety hazard aggravates daily, we should be more concerned about food security and human health.


Recently, subway announced the removal of ADA from it’s bread products. Again, why use an oxidizer like this with risks when there are better alternatives?


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