The article was an interesting read, but I am somewhat confused and concerned about the total absence of the results of DA/AP testing on animals, which are frequently used to determine potential threat to humans. It's all well and good to say "A number of cases of “
Bronchiolitis Obliterans” in popcorn factory workers exposed to DA led authorities to create very strict limits to the amount of DA that workers may be exposed to. It has since been discovered in workers in other manufacturing plants." but that's only part of the story. Those limits weren't based on a handful of workers alone, there were significant medical studies behind the limits as well.
Since this discovery there has in fact been some rather extensive testing of DA and AP exposure to animals, particularly mice, and the results should be made known.
In mice, Diacetyl was tested by vaporizing the diacetyl with an atomizer (sound familiar?) and maintaining a set level within the container the mice were kept in. The mice were exposed to 200ppm to 400ppm (0.02%-0.04%) for 5 days. 5 days of exposure for 24hr/day resulted in necrotizing rhinitis, necrotizing laryngitis and bronchitis, and some deaths. Reducing the exposure to 1 h/day (100, 200, 400 ppm) for 4 weeks resulted in less nasal and laryngeal toxicity, but led to peribronchial and peribronchiolar lymphocytic inflammation. A similar pattern was observed with intermittent high-dose exposures at 1200 ppm (0.12%) for 15 min, twice a day, for 4 weeks. Subchronic exposures to 100 ppm (0.01%) for 6 h/day, 12 weeks, caused moderate nasal injury, and peribronchial lymphocytic inflammation accompanied by epithelial atrophy, denudation, and regeneration. Treatment with 400 mg/kg by oropharyngeal aspiration to bypass the nose caused foci of fibrohistiocytic proliferation with little or no inflammation at the junction of the terminal bronchiole and alveolar duct. Depending on the route and duration of exposure, diacetyl causes significant epithelial injury, peribronchial lymphocytic inflammation, or fibrohistiocytic lesions in the terminal bronchioles.
Similar results were obtained by doing inhalation studies of Acetyl Propionyl in rats. An ongoing two week exposure study caused proliferation of fibrous connective tissue in the walls of airways and projections of fibrous connective tissue sometimes extended into the air passageways. Preliminary data suggests that repeated exposures to either acetyl propionyl or diacetyl can cause airway fibrosis in rats. In the acute inhalation study, changes in gene expression were noted in the brain. Preliminary data suggests that diacetyl can cause changes in the central nervous system. These studies were used as the basis of the CDC's article about flavoring related lung disease.
So it's a bit misleading to only mention the workplace human cases and not include the peer reviewed medical studies when discussing the inhalation safety of these additives. And this was just a small sample of the more than 2 dozen medical studies of this nature done world-wide. It should also be noted that NONE of these studies related to ecigs or vaping, they were studies done based on the safety of the people who worked with these additives and were likely to have significant inhalation exposure. To try to dismiss the results by citing second hand smoking studies is disingenuous at best, If you want to be deliberately misleading, do it to yourself, but do not do it with the safety of others. Otherwise you're no better than the tobacco quacks who tried to prove that smoking tobacco had no ill effects on health whatsoever.