Posted on 06/11/2022 4:14:11 AM PDT by texas booster
10/2/2013 - Can the aroma of peanut from passengers eating peanut on a plane cause anaphylaxis in a peanut allergic passenger?
For those with peanut allergy, there has been a persistent concern about the risk of having a reaction from casual exposure to peanuts while on an airplane. Specific concerns have been raised about reported airborne reactions from inhaling peanut dust or peanut butter vapors or aroma, from being in close proximity to peanuts, or from coming into contact with contaminated surfaces. This is understandable.
However, the peanut allergic flier should rest assured that since the issue was first studied in 2004, data have consistently shown that peanut dust does not become airborne nor does inhaling peanut butter vapors provoke a reaction, that skin contact with either form of peanut is unlikely to cause any reaction beyond local irritation that can be washed off, and lastly that surfaces (including hands) that become contaminated with peanut can be easily washed off. Let’s briefly summarize this evidence.
A 2004 study by Simonte et al. exposed 29 severely peanut allergic patients to a double-blind inhalation challenge to 3oz of peanut butter (or soy butter, both masked for smell) just 12 inches from the nose. As well, a pea sized drop of either masked butter was smeared on the skin for 1 minute, and then was removed. In both exposures, no one developed any allergic reactions. There were 3 patients who developed localized erythema and 5 developing localized pruritus from the peanut butter skin contact, but 5 also developed erythema with soy butter skin contact, which demonstrates that butters on the skin can cause irritation but not generalized reactions.
The authors concluded that casual contact or inhalation of peanut butter was highly unlikely to cause any symptoms.
Also, in 2004, Perry et al. further investigated how effectively 5ml of smeared peanut butter could be abated from tabletops, counters, desks, water fountains, and from one’s hand; and if peanut dust from deshelling peanuts and then walking on their shells could be detected in the air. They noted that multiple commercial agents such as Formula 409, Lysol and Target brand cleaner (containing bleach) removed peanut from surfaces, and Tidy-Types wipes, Wet Ones, and both liquid and bar soap removed peanut from hands. This study also importantly showed that alcohol-based hand sanitizers did not remove peanut from hands, an important staple of how we advise patients.
Most importantly, no airborne peanut was detected in filters worn at the level of the neck from the deshelling experiments. Investigators concluded that peanut can be abated from surfaces with multiple agents, and that peanut dust likely doesn’t circulate in the air.
In 2013, baseline work by the LEAP team as part of home monitoring for compliance with their trial further replicated the findings of both Simonte and Perry. Brough et al. noted that peanut smeared laminate and wood tables vigorously cleaned with a standard commercial cleaning detergent held levels of peanut just above the assay’s detectable threshold (<0.2ug), but that granite surfaces had undetectable levels. Airborne exposure was tested above active and just-halted shelling as well as above baked and pan cooked products. They noted that at 1cm and 1m above peanut being actively shelled, 331ug/m3 and 4.7ug/m3 peanut was detected (assay lower limit of detection being 2.5ug), respectively, but as soon as the shelling was ceased no residual levels were noted at either height.
Thus, these data show that if you put a probe right over someone shelling peanut, a small amount of dust can naturally be detected, but within a few feet only a few nanograms were detectable, likely attributable to the highly sensitive nature of the detecting probe.
These became immediately undetectable once the shelling stopped, and investigators concluded that it is highly unlikely that peanut particles remain in the air after shelling.
In 2016, Jin et al re-replicated these findings within a cabin of an airplane in flight. They noted surface contamination of Ara h 2 on unwashed tray tables after someone ate peanut over them, and among 7 air filters measuring Ara h 2 content when placed on a tray table directly below the mouth of someone eating peanut only 1 filter detected any level, which was 1-2ng/500cm3. They found no detectable peanut levels from 3 air filters tested in a restaurant where individuals were deshelling and eating peanut.
Investigators concluded that the risk of exposure to peanut on an airplane stems from potentially contaminated surfaces and not from airborne levels.
Putting the aggregate of these data into perspective would imply that peanut products likely could be detected on a tray table, common surface, seat, and on the floors if these areas are not cleaned but that there is an exceptionally low likelihood of any airborne circulation. Caution is also needed to rectify what the significance of a few nanograms of detectable protein means - these probes used by Brough and Jin are highly sensitive and can detect exceptionally miniscule amounts. However, these levels are well below any known or theorized level that would be likely to affect even the most highly sensitive patient. Three recent studies have shown that less than 5% of the peanut allergic subjects develop objective symptoms to ingestion of less than 1.5-1.95mg of peanut protein: for reference 1 nanogram is 0.000001mg.
The point here is not to focus on the evolution of more highly sensitive detection methods, but rather to address the more practical issue - that detection of increasingly minute quantities has no clinical relevance. More importantly, the main concern should be on the surface contamination and not airborne particulate. Tray tables and personal seating areas on an airplane should be wiped down, and a 2013 study noted that peanut allergic fliers who reported wiping down their tray tables had significantly lower odds of having reported an allergic reaction to peanut occurring in flight.
It is difficult to understand the context of the reported airborne exposures noted in the 4 studies of self-reported airline reactions, including those addressed in our 2012 response to this question. The limiting feature of these data is that the mechanism of these reactions was not validated by a medical provider, so there is no way to determine what exposure may have occurred, and how. This is not to be confused with their being doubt that a potential reaction occurred. The issue is more through what means, which in the context of this discussion makes all the difference. Thus, these remain in the realm of anecdotal though concerning evidence, and they have been the incentive for the aforementioned studies of surface and air exposure.
The bottom line is that flying with a peanut allergy and being exposed to potential sources of peanut in the cabin is not likely to represent an increased risk to the peanut allergic flier. There is no evidence to support peanut vapor as a cause of reactions or that peanut dust itself circulates and causes reactions. There is evidence that common surfaces on an airplane may have residual peanut contamination, but there is also evidence that this can be readily cleaned with commercial agents that passengers can bring aboard themselves, and that doing such cleaning has been noted to reduce the risk of reporting an in-flight reaction.
In the thread I found several links to medical papers and decided to post a link to this discussion from the AAAAI.
I think we can all agree that the Daily Mail headline accomplished its goal of creating reader clicks, not necessarily dispensing truth.
Now let's look at the science behind it.
...it is dedicated to Established in 2011, SnackSafely.com provides straightforward, actionable information to help improve the lives of the estimated 32 million people in the US suffering with food allergies.
14-Year-Old Girl Suffers Anaphylaxis Aboard BA Flight After Passenger Refuses to Stop Eating Peanuts
Prevention
According to recent studies, there is strong evidence that introducing at-risk babies to peanuts as early as 4 to 6 months of age may reduce their risk of developing food allergies by up to 80%. Babies at risk for peanut allergy include those with mild to severe eczema, egg allergy, or both. Before introducing your baby to peanuts, discuss the best approach with your child's doctor.
So we are learning more and more about how to prevent allergies in children, and keeping children away from peanuts for the first year of life does not seem to help.
Before the first description of hay fever in 1870, there was very little awareness of allergic disease, which is actually similar to the situation in prehygiene villages in Africa today. The best explanation for the appearance and subsequent increase in hay fever at that time is the combination of hygiene and increased pollen secondary to changes in agriculture. However, it is important to remember that the major changes in hygiene in Northern Europe and the United States were complete by 1920. Asthma in children did not start to increase until 1960, but by 1990, it had clearly increased to epidemic numbers in all countries where children had adopted an indoor lifestyle. There are many features of the move indoors that could have played a role; these include increased sensitization to indoor allergens, diet, and decreased physical activity, as well as the effects of prolonged periods of shallow breathing.
Since 1990, there has been a remarkable increase in food allergy, which has now reached epidemic numbers. Peanut has played a major role in the food epidemic, and there is increasing evidence that sensitization to peanut can occur through the skin. This suggests the possibility that changes in lifestyle in the last 20 years could have influenced the permeability of the skin. Overall, the important conclusion is that sequential changes in lifestyle have led to increases in different forms of allergic disease. Equally, it is clear that the consequences of hygiene, indoor entertainment, and changes in diet or physical activity have never been predicted.
Very long article but also excellent. Looking at the sudden increase in allergies and asthma since 1960.
Table IV - Pre-existing factors and changes that could be relevant to the increase in peanut allergy in the United States, 1990 to the present
I. Differences in the preparation of peanut products
A. Roasted vs boiled
B. Emulsified peanut products in the United States
II. Delayed oral consumption of peanut proteins
A. Comparison of Israel and London
B. American Academy of Pediatrics policy regarding avoiding peanut products
III.Changes in skin as a result of daily bathing with soap or detergents
A. Removal of lipids from skin
B. Other damage that could allow increased skin penetration
IV.Changes in vaccination policy
A. Increase in frequency
B. Change from cellular to acellular pertussis
More food for thought.
The epidemic increase of asthma among children: 1960-2000
Before 1960, most pediatrics textbooks did not regard asthma as common, let alone epidemic. During the 1960s, there were occasional reports that asthma appeared to be becoming more common, but the first convincing publication came in 1969. Smith et al, carried out a population-based study on schoolchildren in Birmingham, United Kingdom, which demonstrated a sharp increase in asthma between 1958 and 1968. In addition, they reported that many of the children with asthma had positive skin test responses to dust mites. Over the next few years, reports on the increasing prevalence of asthma came from several countries but predominantly from countries in which dust mites were the dominant allergen. Thus increases were reported from Australia, New Zealand, and Japan, as well as the United Kingdom.
Indeed, by the 1980s, it was possible to argue that increasing growth of dust mites in houses was an important cause of the increase in asthma.
That argument was helped by the fact that homes in the United Kingdom, Australia, and New Zealand had become warmer and tighter and had more carpets. In turn, this was thought to have provided improved conditions for the growth of dust mites and for the accumulation of debris from dust mite growth.
However, it is important to recognize that a large part of the reason for wanting homes warmer and less drafty was because of the increase in indoor entertainment.
Although it is well known today that asthma has increased in all Western countries, it might be forgotten that this did not become clear until 1990. In that year, data on asthma among recruits to the Finnish and Swedish armies came out, showing a progressive increase over 20 years.
However, in large parts of Sweden, the dominant allergens associated with asthma are those associated with cats or dogs.
In addition, evidence was accumulating that cockroach was a major allergen related to asthma among African Americans living in poverty in the United States.
By 1995, it was accepted that both the prevalence and hospitalization for asthma had increased among children living in climates or living conditions in which several different allergens dominated both exposure and sensitization.
At this point, it became very difficult to argue that the increase had occurred simply because of an increase in allergens in homes because there was no reason to think that dust mite, cockroach, cat, and Alternaria species had all increased in parallel. It is important to recognize that the best evidence about the role of allergens in asthma came between 1970 and 1980, with convincing demonstrations that chronic allergen exposure could make a major contribution to nonspecific bronchial hyperreactivity (BHR).
Any attempt to explain the increase in pediatric asthma has to deal with the progressive nature of the increase. Although major changes were present by 1980, the increase continued for at least 2 more decades. Although there is evidence for many different aspects of the increase in asthma prevalence and severity, most of these arguments cannot explain either the time course or the scale of the increase (Fig 3).
A typical example is the change from aspirin to paracetamol in 1979 after the identification of Reyes syndrome. This change might well have contributed to the severity of asthma but did not occur until halfway through the increase.
In most studies asthmatic children were found to be allergic to 1 or more of the common perennial allergens. In Australia Peat and Woolcock reported detailed studies on the “modifiable risk factors for asthma,” including diet and immunization, and they concluded that dust mite allergy was the most important of these factors.
Taking everything into account, the changes that fit the time course best are the ultimately disastrous changes that occurred after the introduction of television programs designed for children in the 1950s (Table III). There are 3 questions that need addressing in relation to this period:
1. Were there changes in hygiene during this period that could explain the timing, scale, or severity of the increase in asthma?
2. Could decreased physical activity or simply changes in breathing patterns secondary to sitting and watching a screen have had a major effect?
3. Could any of the other changes, including obesity, increasing schedules of immunization of children, and the change from aspirin to acetaminophen, explain more than a minor part of the epidemic?
Table III Changes that have been suggested as explanations for the progressive increase in pediatric asthma, 1955-2000
I. Increased number of immunizations in early childhood and possible changes in vaccines
II. Progressive increase in the use of broad-spectrum antibiotics
III. Use of paracetamol to treat fever in childhood, which replaced aspirin, after identification of Reyes syndrome in 1979
IV. Changes that occurred either because of or in parallel with the introduction and increase in indoor entertainment: primarily television programs for children, 1955 onward:
A. Decreased play outdoors with consequent decrease in exposure to bacteria and decreased physical activity
B. Progressive increase in body mass index among children
C. Changes in homes to increase comfort, including decreased ventilation, increased carpeting and furnishing, and increased temperature
D. Changes in breathing patterns while watching television, including decrease in sigh rates
V. Increased exposure to indoor allergens secondary to less time outdoors and higher quantities indoors
Could number VI be hysteria?
We have a friend who just completed a one week stay in the hospital from aspergillus poisoning. She was at death’s door. Peanuts are by far the major carrier of aspergillus fungus.
Aspergillus develops in peanuts grown in too-wet conditions, in un-drained soil, or during periods of excess rain. I suspect that many cases of peanut allergy are associated with aspergillus exposure.
The FDA stopped monitoring or correcting aspergillus in peanuts years ago, and cases of aspergillus poisoning have increased ever since that time. I suspect that imported peanuts is the reason why the FDA dropped peanut monitoring. Peanuts with a minor case of aspergillus can develop major cases of aspergillus during days in the holds of ships.
Generally, peanuts with aspergillus look less healthy than peanuts without aspergillus. However, peanut consumers don’t get to inspect peanuts before they get ground into peanut butter. It would be natural to assume that peanut butter manufacturers would use these cheaper peanuts in making peanut butter.
Next we can move into the recent rise in ergot contamination found in northern barley lately.
Munchhausen by Proxy is not unheard of, and in this case, the Mom got her 15 minutes of fame and the daughter made her Mom happy.
But impossible to tell from a distance.
(Not that it ever stops anyone)
Not dissimilar from the corn tortilla poisoning affecting infant brain growth in the ... 80’s? 90’s?
I wonder how many of today’s health issues will be found to be due to government negligence ... or being sold out to the bio-industries (including many patented hybrid seeds we use) ... and the Big Pharma/Government complex.
Regards,
I’m looking forward to reading this article later today when the “But I....” crowd gets on with all their unprovable stories.
Here’s mine. A few years ago I helped coach a youth robotics team. One kid had supposedly horrendous peanut allergies but the parents didn’t make a big deal about it.
During the build season the team spent countless hours at the shop, often 6-8 hours every night and 10-15 on weekends.
Snacks were common. Someone brought in a 5 lb bag of peanuts in the shell. There were peanut shells all over the place. The kid was completely unaffected because he didn’t actually eat any of them.
A couple years later, a kid joined another youth group I worked with. Mom warmed up her helicopter and sat us down to tell us how deadly peanuts would be to her 11 year old kid. At one point I asked if they ever did the peanut test at a hospital, where he would check in, eat a handful of peanuts and see what happened. “Oh no. I would never subject my son to something that harmful.” She’d rather punish him with fear that he would die if he took the wrong breath.
We later established that it had been nine years since he’d had a reaction.
Many parents would rather make their kid live in fear and lots of doctors are more than happy to keep the money train rolling in and stoke that fear rather then check to see if he grew out of it. (like my kid did back before peanut allergies were a thing)
Reactions to peanut during air travel: can anaphylaxis be due to inhalation?>>. I would say yes as there are just masses of people dying on airplanes./s
Bless you for sponsoring a robotics team, especially in the old days. Seems easier nowadays.
We have seen the same fearmongering with Covid and kids. Have met kids that just won’t be outside without a mask.
Whatever happened to sunlight being a disinfectant and fresh air being healthy?
The girl probably ate a peanut and mom now wants to sue the airline.
what stands out to me is the mommy was able to see a person eating peanuts 10 rows up.
Is she 10 feet tall? When i have flown i can barely see the tops of the heads of the folks in front of me, much less what they are eating or drinking.
I’m 80 years old. I took a PB&J sandwich to school EVERY day because that’s what we could afford. I often shared/traded my sandwich with some other kid who had something different like tuna fish or bologna just to vary my lucnches.
To my knowledge there was never a trail of dead children leading to my sandwiches. So something has changed within the world of peanuts. or within the world of children???
To be fair, the FDA’s biggest obstacle in eliminating peanut aspergillus came from domestic peanut farmers. The FDA would test samples of a crop. If the samples measured over a threshold concentration of aspergillus then the FDA and county ag agents would order the crop destroyed. Periodically farmers would file lawsuits to enjoin the destruction orders. Farmers started winning more and more of the lawsuits.
When large foreign peanut supplies started showing up the totality became too much for the system to handle, so they shut it down.
Peanut aspergillus is like ergot in rye and barley. It’s been known about for decades. The problem lies in doing something about it.
Well. There it is.
NOW I know why I’m not allergic to peanuts; I was practically born with a PBJ sandwich in my mouth.
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