Allergies in Young Children: Effects of Exposure to Multiple Air Pollutants During Prenatal and Early Life
By Roberta Attanasio
The frequency of allergies in children keeps rising rapidly worldwide, but it’s not clear why. However, it is acknowledged that developing even one type of allergy early in life is almost like turning on a switch—it can start children on a path to more. “The progression of skin allergies to asthma and allergic rhinitis is called the allergic or atopic march. Atopic dermatitis is an itchy, inflammatory skin allergy that, before 1960, affected fewer than 3% of children; by the 2000s it had increased to around 20%. A child with atopic dermatitis is more likely to develop other allergic conditions or symptoms. For example, about 70% of people with severe atopic dermatitis have asthma, whereas in those without atopic dermatitis, only about 8% have asthma—a nearly 9-fold difference.”
According to the American Academy of Allergy, Asthma & Immunology, atopy refers to the genetic tendency to develop allergic diseases such as allergic rhinitis, asthma and atopic dermatitis (eczema). Atopy is typically associated with heightened immune responses, more specifically with excessive IgE production in response to common allergens, especially inhaled allergens and food allergens.
Atopic diseases (eczema, asthma and rhinoconjunctivitis) are clinical syndromes each defined by a group of symptoms and signs. Not all children with atopy will have atopic disease or develop symptoms after exposure to an allergen. Both genetic and environmental factors determine the development of atopic disease.
Now, results from a new study show that there is a significant association between multiple prenatal and early life exposures to indoor pollutants and the degree of allergic sensitivity in 2 year old children.
For the study, researchers followed 108 mother-child pairs from birth to 2 years of age. They obtained data on the exposure to air fresheners, candles, mold, cats, dogs, carpet and environmental tobacco smoke during the prenatal, 6-month, 1-year, and 2-year timepoints. Then, they performed a skin prick test on both the mother and the 2-year-old child. A skin prick test, also called a puncture or scratch test, checks for immediate allergic reactions to as many as 40 different substances at once. This test is usually done to identify allergies to pollen, mold, pet dander, dust mites and foods. In adults, the test is usually done on the forearm, whereas children may be tested on the upper back.
The researchers found that exposure to candles during the prenatal window, cats during the 6 month window, and environmental tobacco smoke at 2 years significantly increased the risk of a positive skin prick test, thus supporting the role of the indoor environment on the development of atopic disease. They also found that combined effect of multiple exposures may be more influential to allergy development than one single exposure.
Anne Ellis, one of the study authors, said: “The increase in the average amount of time indoors means there is an increased risk of harmful health outcomes related to exposure to indoor air pollutants. Additionally, children breathe more frequently per minute than adults, and mostly breathe through their mouths. These differences could allow for air pollutants to penetrate more deeply into the lungs and at higher concentrations, making children more vulnerable to air pollutants.”
Exposure to air fresheners and candles is of particular interest, as they contain phthalates, ubiquitous pollutants with wide-ranging negative health impacts. Previous work by the same researchers had already established that indoor air freshener exposure is associated with respiratory symptoms at 2 years of age.
While noting comments during the ongoing Flint lead pollution problems, it was often stated that even though lead levels in drinking water were elevated above unsafe levels, that bathing with such water was okay ‘because lead does not pass through the skin’.
I was concerned that this was encouraging lead exposure to skin, even though I had remembered reading a paper in 1994, by Stauber and Gulson, that seemed to point out that contrary to ‘common’ knowledge, lead can fairly readily pass through skin, yet not result in increased blood lead levels. Many the Flint population that did continue to shower in Pb elevated water persistently complained about severe rashes, yet were not taken very seriously by authorities because of the long held assumption that lead did not pass through skin. I did a literature search that resulted in finding a number of papers since the original 1994 paper.
It may be true that substantial research supports the safety of bathing in high lead water, but scientists should cite the papers that indicate that bathing would be alright. The following citations might suggest that perhaps lead may pass through the skin under such practices as bathing. Other research might beg to differ…. but we should have authorities cite the research that they think supports their position…given the research below.
Notes: re: skin exposure potential uptake of Pb without much indication from subsequently elevated blood lead testing.
Lilley SG, Florence TM and Stauber JL. The use of sweat to monitor lead absorption through the skin. Sci Total Environ. 1988;76(2-3):267-78.
Stauber JL, Florence TM, Gulson BL and Dale LS. Percutaneous absorption of inorganic lead compounds. Sci Total Environ. 1994;145(1-2):55-70.
Sun CC, Wong TT, Hwang YH, Chao KY, Jee SH and Wang JD. Percutaneous absorption of inorganic lead compounds. AIHA J. 2002;63(5):641-6.
Stauber JL, Florence TM, Gulson BL and Dale LS. Percutaneous absorption of inorganic lead compounds. Sci Total Environ. 1994;145(1-2):55-70.
Marzulli FN, Watlington PM and Maibach HI. Exploratory skin penetration findings relating to the use of lead acetate hair dyes. Hair as a test tissue for monitoring uptake of systemic lead. Curr. Probl. Dermatol. 1978;7:196-204
Skin Absorption of Inorganic Lead (PbO) and the Effect of Skin Cleansers.
Journal of Occupational & Environmental Medicine. 48(7):692-699, July 2006
Filon, Francesca Larese MD; Boenigar, Mark MD; Maina, Giovanni MD, Adami Gianpiero PhD; spinelli, Paolo MD; Damian, Adriano MD
Objective: The aim of this study was to investigate the percutaneous penetration of lead oxide (PbO) powder and the effects of rapid skin decontamination with two different detergents.
Methods: Franz cells were used to study in vitro PbO skin penetration through human skin during a 24-hour period. The tests were performed without or with decontamination using either Ivory Liquid soap od a new experimental cleanser 30 minutes after the start of exposure.
Results: we confirm that PbO can pass through the skin with a median penetration of 2.9 ng/cm2 (25-75th percentiles 0.35-6). The cleaning procedure using Ivory Liquid soap significantly increased skin penetration with a median value of 23.6 ng/cm2 (25-75th percentiles) 12-47.1; Mann-Whitney U test, P= 0.0002). whereas the new experimental cleanser only marginally increased penetration (7.1 ng/cm2).
Conclusions: Our results indicate that it is necessary to prevent skin contamination from occurring because a short contact can increase skin content and penetration even if quickly followed by washing. This study demonstrated that PbO powder can pass through the skin and that skin decontamination done after 30 minutes of exposure did not decrease skin absorption occurring over 24 hours and stresses the need to prevent skin contamination when using toxic substances.
© 2006 The American College of Occupational and Environmental Medicine
Note: the citation (Stauber et al. ’94) apparently found that, contrary to common thought about percutaneous uptake of Pb, lead can often pass through skin. Apparently this route also causes the Pb to have greatly reduced affinity for red blood cells. This then results in non-detect tendency in blood lead testing. Could this loss of affinity for the red blood cells be the reason that so many other toxicology references claim that the skin route of Pb exposure is NOT very much of a factor? Has this belief caused poor study designs to mask the actual risk from skin absorption of Pb? Regulatory agencies were probably happy to not have to worry much about this potential route of Pb uptake, and so perpetuate the apparent misconception…. which other researchers then assume to be correct when they go to design their new studies… and potentially reach erroneous conclusions about the efficacy of the skin uptake route. Any failure to see much of an elevation in blood lead testing would just affirm their underlying assumption.. ..that just might be erroneous. You often don’t find what you don’t look for.
If this assumption pervades lead research and lead regulatory paradigms, there should be some more pointedly investigative clarification of the validity of the work previously done in the above research citations. IMHO
It appears that this could question a lot of assumptions in best management practices that lead exposure through skin is not very significant… including soil lead handling during urban gardening and subsequent hand cleansing protocols needed to prevent hidden uptake that might not even register upon well done blood lead testing that is supposedly the definitive assessment.
Lead is known to adversely affect calmodulin, an important defensive component in skin. Many communities, beyond Flint, have similar lead contaminated water, how many people are bathing frequently, and having skin problems?
Because of the prevalence of atopic disease in our modern world, it is imperative to discuss it, as most of us are around the age where we either have siblings who may be affected by these immune system disorders, or we have children or are planning to have children of our own, and even more simply just becoming we are sensible to the health of people that are closest to us. I thought the research was fascinating because we have sedentary lifestyles, therefore we stay indoors for the majority of the day, which can account for exposure to indoor pollutants. This simple practice in our lives predisposes us to many diseases such as atopic disease. One study I found supported the same arguments. Conversely, another study suggested that exposure to fungal and bacterial pollutants in moderation during early childhood can result in reduced risk of developing specific allergic sensitizations to aeroallergens. Lastly, a more recent study done in 2018 (https://www.nejm.org/doi/full/10.1056/NEJMoa1804092) was making novel new immunotherapy drugs to combat atopic disease in adults and is currently being tested for pediatric use. The mechanism of action Dupilumab is an IL-4 inhibitor. This is an important marker that is characteristic of Th2 cells that are closely linked to the integral proccess of an allergic response. By blocking the receptors that respond to IL-4 it stops the process at the very top. A normal cell to cell to cell communication needs the T-cell to differentiate into a Th2, that secretes IL-4 and IL-5 to communicate with more cells. IL-4 from Th2 binds to receptors of B-cells to undergo class switching to secrete IgE isotype instead of IgM. These B-cells create a memory with their specific IgE antibodies, and for next exposure, the cells have already undergone sensitization, so the response to an allergen is much faster. IgE antibodies have a unique characteristic compared to the other immunoglobulins that allow them to bind to their Fc regions to mast cells, where they get cross-linked by an antigen and cause them to degranulate. It is because of this process that these IgE antibodies have such a quick response to subsequent exposures to allergens because IgE are already bound to mast cells, ready for a response. Th2 differentiated cells also secrete IL-5 that signal to eosinophils, another cell that contributes in a type 1 hypersensitivity reaction. Hence why this drug is so promising, it is a fully human monoclonal antibody that targets the IL-4 alpha receptor on T-cells, that inhibit them from differentiating into active Th2 cells. I think it will be interesting to see what direction this immunotherapy takes us in future medicine because its efficacies have been proven, but the current cost is for $46K per year.
Very interesting read! The first thing that was shocking to me was the fact that developing one allergy immediately opens the path to developing more. I find it very alarming, and worthy of further research. It is definitely concerning that not even in one’s own home can you be kept safe from things such as contaminants. I had no idea that simple things like air fresheners could lead to development of allergies. The question becomes, if these things are known to trigger health issues, why are phthalates still being used to produce these air fresheners?
I was particularly interested in the negative effects that phthalates have on the body and what conditions its can contribute to. I found a research paper written by Kim et al. that discusses the link between atopic dermatitis (AD) symptoms and exposure to two endocrine disrupting chemicals (EDC’s), phthalates and bisphenol A (BPA) in children. The study followed the progression of symptoms through normal daily exposure to these chemicals in 18 boys with AD, all ages 3 to 7 years, throughout one year. Morning and afternoon urine samples were analyzed for phthalate (MnBP, DnBP, and BBzp) and BPA (BPAG) metabolites. Interestingly, AD symptoms were strongly correlated with an increase in phthalate metabolite levels on the same day. Furthermore, all phthalate metabolites measured correlated with the levels of BPA metabolites. This data suggests that both phthalate and BPA metabolites must have an effect on the development of AD symptoms. BPA not only seems to be associated with AD but also with allergic asthma as it seems to induce IgE responses. I think that with research like the one discussed here is important for the development of household products that deviate away from the use of phthalates and BPAs. Most of our exposure to these EDC’s is within our home and these contaminants can even be found in dust. This is especially alarming because young toddlers who have an urge to touch everything and put everything in their mouth have a higher risk of ingestion and inhalation of these EDC’s within one’s own home. I definitely think that regulation of these chemicals needs to be implemented to avoid such common exposure.
Not only does exposure to phthalates and BPA have an effect on the development of AD symptoms but this study I found by Singh and Li shows how exposure to phthalates and BPA in mice lead to epigenetic changes correlated with the development of cancer. In their study, the effect of BPA lead to an epigenetic change to a gene known as EZH2. The overexpression of this gene has been shown to lead to cancer by down regulating tumor suppressing genes. Not only does BPA have epigenetic effects but the study also found that phthalates have similar effects. More alarmingly, the study found that these epigenetic effects can be passed down through generations. The study also mentions that biomonitoring of BPA through urine testing may actually be underestimating the amounts of BPA in the total body. After reading this study along with your comment, I totally agree with you that limiting our exposure to these endocrine disrupting chemicals and finding alternative products is an important topic.
The effects of air pollutant exposure on allergies in young children is such an interesting subject. I had no idea there was a connection between atopic dermatitis and asthma, but now that I think about it the two friends I have with asthma also have eczema. In fact, one of those friends is also allergic to peanuts, shellfish, tree nuts, bees, pollen, mold, and the list goes on. Maybe her allergies were caused by an increased exposure to indoor pollutants at a very young age like the study presented in the article suggests. This article made me wonder about the barriers of immune defense that may have been broken down by environmental toxins at an early age to cause increased sensitivity to allergens. Since the first barrier of defense is the skin and atopic dermatitis is the beginning of the atopic march towards asthma and allergic rhinitis, I wondered if there is a correlation between the two such that the skin may be the primary immune system defect that initiates the body’s progression toward allergies. I did some more research on the atopic march and found a paper by Zheng et al. that examines current research on the interplay between immunological function including the epithelial barrier and environmental toxins. The paper shows that the influence of the environment on genetic factors is complicated and does not result in a neat, linear progression from one disease to another (atopic dermatitis to asthma). The review also states that food allergies are known to provoke atopic dermatitis. 35% of children with atopic dermatitis have IgE mediated food allergies. Affected children have increased IgE production, causing increased sensitivity to environmental pollutants. This added information makes me curious about food allergies’ relationship to the atopic march. I am curious if there is an IgE threshold that stimulates the onset of a new allergy in the progression of atopic diseases. Maybe the sensitivity threshold is lower for contact and ingestion than for inhalation of allergens, leaving asthma at the end of progression. This would be a great area for further research.
Please refer to paper’s link below for more information.
I thought it was interesting that they were specifically looking at mostly pollutants that were considered indoor. In the paper that I found to follow up this post, it made a good point as to why the indoor pollutants are more important to the age of the children in this study. Smaller children spend most of their life and daily time inside their home so this is the environment that is really going to have an impact on their AD and health. In the homes of the families that were studied, the major culprit for the majority of the air pollution found was due to candles, cooking, and other ways that use combustion. They did study a lot of the same pollutants used in the study for this post. Following up with the tobacco finding in the article for the post, my article I found supported the finding. The development of AD during the child’s first year of life can be affected by the level of recruitment of immune cells that are responsible for allergy response (basophils and eosinophils) due to exposure to tobacco smoke. I did find it interesting that this article discussed a fungus that can be contracted by pets that may be in the household and that the use of an air purifier/cleaner can reduce the concentrations of the bacteria aerosols. I think that these air cleaners are a good treatment, in a sense, to help cut down on the level of pollutants found in the home.
This is a very fascinating topic as it proves to show that maternal exposure to environmental contaminants on a developing fetus’s immune system plays a significant role. We have discussed that the skin is the first line of defense, and data suggests that the manifestation of allergic disease in children primarily presents as atopic dermatitis and asthma. I am interested in understanding the correlation between our innate immune system during these two very different symptoms and how this is potentially influenced by maternal exposure to environmental factors prenatally. In a study conducted by Ashley-Martin and others, they looked at the effects of nitrogen dioxide exposure throughout the pregnancy. The correlation they found is that both symptoms are associated with an increase in epithelial cell-derived cytokines which plays a role in type 2 inflammation of epithelial cells lining the skin and respiratory tract as well in the regulation of innate and adaptive immunity. As a biomarker for infant allergic disease they looked at IgE, IL-33, and TSLP (immunoglobulin and cytokines) in the placenta cord blood upon exposure to increased areas of NO2. This data suggests that maternal exposure to environmental toxins, such as NO2, is crucial to the early development of the immune system function; even in utero as these cytokines are most likely not maternal but instead from the developing fetus itself. Lastly, the data shows that exposure during the third trimester increases cytokine levels in the cord blood compared to the first, which may be valuable information in understanding what preventative measures can be adapted in an area of high pollution to lower the risk of allergic disease in children.
It definitely is astonishing how so many factors can impact the development of disease and allergy even in utero. It’s truly concerning that exposure to the mother can have detrimental effects on the health and immunity of a baby after birth. As you mentioned, nitrogen dioxide and other environmental pollutants often have an effect on the development of immune system function. This got me thinking, what about deficiencies during gestation and after birth? I found an article by Vasiliou, J.E., et al that discusses some of the effects of vitamin D deficiency on the immune system of mice offspring. Previous research had found that lower serum vitamin D levels were associated with poor lung function and that low levels led to increase sensitivity to aeroallergens. The research paper I found studied in utero and early-life vitamin D deficiency using a mouse model. Female mice were fed either a vitamin D deficient diet during gestation or normal diet and after birth, the pups were also fed a vitamin D deficient diet or normal diet. The pups were then exposed to house dust mite (HDM). Results showed that a vitamin D deficient diet led to an increase in pulmonary Th2 cells and reduced Treg Cells. Eosinophilia in lungs were high in vitamin D deficient diets in utero and after birth, but reduced greatly after vitamin D supplementation was provided after birth. Furthermore, it was found that in pups who were fed a vitamin D supplemented diet after birth, there was a significant reduction in the IgE present after exposure to HDM compared to the amount of IgE present in pups exposed to the same allergen, but fed a vitamin D deficient diet. Thus we can see that vitamin D deficiency modifies immunological responses to allergens through Th2 skewed response and eosinophilia. Knowledge of the immunomodulating activities of vitamin D allows us to dive deeper into research about potential vitamin D supplementation in treatments used to reduce severity of allergic responses.
Yes, just contemplate low Vit D 3 levels seen with poor outcome in ICU of COVID 9 patients, association yes, causation a good question, especially since it is hormonal in many effects.
I was very surprised to learn that common household items such as candles and air fresheners, available readily in stores for any age to buy, can have detrimental effects via allergies, especially in those younger of age. So not only does the type of allergen determine disease state, but also the age at which children are exposed to particular allergens. This creates an interesting situation for the potential for allergies to develop in children, considering many families have dogs, cats, and other small mammals as members of their family, and items such as candles and air fresheners are governmentally approved for sale. According to the attached study, not only does the age at which one is exposed to a specific type of allergen have an effect, but also once exposed and disease state progresses, allergies can present themselves and progress as age progresses. It is noted in the study that young children between the ages 5 and under are more likely to have allergens lead to atopic dermatitis, but ages up to 9 years are more likely to experience asthma, while it seems the allergic disease progresses to allergic rhinitis between ages 6 to 11 years. So not only does the type of allergen play a role in disease state, but also at what age the person is exposed to the allergen, and the allergic disease can further progress and present itself in different forms as age increases.
That’s a really good point, now taking what you said my question is that is there a way to improve asthma and allergies in children since exposure is almost inevitable; because like you said many family have animals, candles, and air fresheners in their household, so It is almost impossible to just completely get rid of it all. One study I found suggests possible environmental interventions. For asthma interventions researchers suggested mechanical methods including impermeable bedding, ventilation, frequent cleaning, central heating, pest control methods, and even possibly better educating parents of children with asthma and allergies. They found that a combination of these methods, like better ventilation throughout the household combined with frequent cleaning using a high-efficiency particulate air (HEPA) vacuum, showed airborne allergens were captured by the cleaners and the airway hyper-responsiveness of children significantly decreased. Education of parents with asthmatic children has shown mixed results meaning it was up to the parents for how to care for their children with severe allergies and asthma. Overall, mechanical interventions in the home have shown a huge improvement in reducing asthma and allergen triggers. But, combining educational and mechanical methods can significantly decrease asthma attacks and allergic reactions. I do believe there can be more research done on intervention methods that can be more cost friendly and for more methods to be developed to improve asthma and allergies that develop in children that can’t help exposure.
I found this post to be thought-provoking and fascinating as I was not aware of the recent influx of children’s allergies. The mention of phthalate exposure via candles and air fresheners was of particular interest to me because candidly, I use these products in my home religiously so I wanted to become more versed in the literature. I personally do not suffer from asthma but I have family members that are affected. This made me ponder on whether or not there are studies that show an association between phthalate exposure and asthma. I found one study that investigated the association of phthalates exposure with pulmonary function and airway inflammation in asthmatic children. In this study 46-Korean children with asthma were observed over a two-year period. The study looked at urinary levels of various phthalates, expiratory volume in 1 sec (FEV1), peak expiratory flow rate (PEFR), and the fractional exhaled nitric oxide (FeNO) as a marker of airway inflammation. The results showed an increase in phthalate metabolites was associated with a decrease in pulmonary function and an increase in airway inflammation (FeNO). This illustrates that phthalate exposure may exacerbate symptoms of asthmatic children so exposure should be minimized.
After reading your post and then following up with the study that you linked, Prenatal and early life exposure to indoor air-polluting factors and allergic sensitization at 2 years of age (M.J Gallant et. al. 2019), I can not help but to see more of the microbiome at work. In the studies’ own discussion, they mention that both the exposure to dogs, carpet, but not cats decreased the prevalence of the allergies in children at the two-year mark. Each of these “allergens” host many different commensal microbes whose effects are still not fully understood, and yet some of these microbes can cause a lot of harm, like histoplasma in cats. Who can say that exposure to these microbiomes are not directly linked to the immunity itself?
Through additional reading I have found a letter in The Journal of Allergy and Clinical Immunology by A.C. Ouwehand et. al that suggests a links between atopic disease with a higher incidence rate in infants that were colonized by high levels of adultlike Bifidobacterium at a young age, and an inverse for infants colonized by Bifidobacterium adolescentis. Though the number of infants the study was able to test were low, it shows the possibility of specific species of bacteria both causing and negating allergic reactions in children. Such relationships can be the missing link for the cause of increased allergy diagnosis rates described by the American Academy of Allergy Asthma and Immunology’s “hygiene hypothesis”.
I think studying what microorganisms could potentially also be driving the symptoms of atopic dermatitis and asthma in young children in correlation to environmental pollutants is worth exploring, especially for treatment. In addition, I think something that could potentially be utilized as a control in studies is to look at how essential oils could play a role in the immune system and allergic diseases in children. Essential oils often have antimicrobial properties, therefore reducing the risk of an immune response caused by microbes, and also we see the use of essential oils in many candles and diffusers. So this type of study may be useful in looking at the direct effects of environmental pollutants without worrying about the effects of microbes but it may also suggest that essential oil use is potentially harmful/beneficial to the developing immune system if it were to be used as an antimicrobial agent or fragrance. In a study by Sharma and group, they looked at the use of essential oil Angelica glauca which in traditional medicine has been used for treatment in bronchial asthma. In a study with guinea pigs they used histamine (which is normally released by mast cells during an allergic response due to increased levels of IgE binding to the mast cells) to mimic a hypersensitivity reaction, and then with these essential oil treated guinea pigs they saw a reduction in IgE and eosinophils which correlates with bronchodilation and decrease in inflammation since cytokines and mast cells were not chronically activated during the immune response. This may suggest that the use of essential oils for candles, air fresheners, cleaning agents, etc. may be better suited for children with active allergic diseases such as eczema/asthma but also may be better to use during pregnancy for the fetus’s developing immune system.
I think studying how microorganisms could potentially also be driving the symptoms of atopic dermatitis and asthma in young children in correlation to environmental pollutants is worth exploring, especially for treatment. In addition, I think something that could potentially be utilized as a control in studies is to look at how essential oils could play a role in the immune system and allergic diseases in children. Essential oils often have antimicrobial properties, therefore reducing the risk of an immune response caused by microbes, and also we see the use of essential oils in many candles and diffusers. So this type of study may be useful in looking at the direct effects of environmental pollutants without worrying about the effects of microbes but it may also suggest that essential oil use is potentially harmful/beneficial to the developing immune system if it were to be used as an antimicrobial agent or fragrance. In a study by Sharma and group, they looked at the use of essential oil Angelica glauca which in traditional medicine has been used for treatment in bronchial asthma. In a study with guinea pigs they used histamine (which is normally released by mast cells during an allergic response due to increased levels of IgE binding to the mast cells) to mimic a hypersensitivity reaction, and then with these essential oil treated guinea pigs they saw a reduction in IgE and eosinophils which correlates with bronchodilation and decrease in inflammation since cytokines and mast cells were not chronically activated during the immune response. This may suggest that the use of essential oils for candles, air fresheners, cleaning agents, etc. may be better suited for children with active allergic diseases such as eczema/asthma but also may be better to use during pregnancy for the fetus’s developing immune system.
This is a very interesting post! All parents should read this post and understand the effects of household pollutants. I am amazed to learn that prenatal exposures such as candles, molds, and cats increase the risk of a positive skin prick test in children. I immediately became interested in prenatal smoking and the development of eczema. A study conducted by Thacer Et. al, followed 4089 children from birth to 16 years. They collected household information through a series of questionnaires. Researchers found that exposure to secondhand smoke in utero increased the chance of developing asthma. Exposure to Secondhand smoke as an infant increased the risk of developing asthma, eczema, and rhinitis. Secondhand smoke has been found to increase the risk of developing allergic disease. These findings are impactful and should encourage the community to prohibit smoking in public areas. All in all, prenatal exposure to pollutants such as candles, molds, and secondhand smoke negatively impact the child’s health outcome. A potential future study could analyze the relationship between prenatal exposure to secondhand smoke and pneumonia in the lungs of children.
It really concerning to see the health implications that arise from different types of inhalants that we as society see as a normal. In addition to the phthalates that come from seemingly harmless household items such as candles and air fresheners, other gaseous compounds cause harm to our immune systems. Recently, vaping has been in spotlight for its harmful immunological effects. Initially marketed as a safe alternative with no side effects for smokers, recent research by B. Reidel et. al. has shown that vaping itself causes the same airway secretions that cigarette smoking initiates. In fact, the sputum collected from e-cigarette users also had elevated markers for neutrophil activation, which is described by the author as a major contributor to the pathogenesis of lung disease in the same way with e-cigarettes as it is with normal tobacco cigarettes. Likely, with other seemingly ubiquitous gaseous compounds, there will be this same relationship that progresses fatal diseases.
I was also shocked that candles could be a culprit in atopic dermatitis studied. You don’t really think about candles being ‘bad’ and causing issues like this since they smell good and never really get bad wraps, at least that is how I feel about it. I never realized how many different environmental factors could have an impact pre-natal via the mother’s exposure. Cigarettes are a given, but I never really put much thought into animals or air fresheners. My article I found discussed how exposure to tobacco smoke in children up to the age of one can influence the recruitment and differentiation of the allergy-related immune cells (basophils and eosinophils) and how this leads to the development of diseases like atopic dermatitis. I agree that this is just another reason for cigarettes to be prohibited more. I would like to look at data regarding air purifiers/cleaners and how they might help mediate some of these issues related to pollutant exposure.
When I first read this article, I became very interested in how the allergies progressed from skin reactions into a respiratory problem such as asthma. Upon doing some research, I found a study that showed that a loss of function mutation in a gene known as filaggrin was found to be present in people who had asthma after having atopic dermatitis. The filaggrin gene helps to create the skin barrier so when its function is lost, the skin barrier is broken leading to the rise of atopic dermatitis. This can then lead to asthma because after the first exposure to the allergen, such as dust mites or phthalates, the protective skin barrier breaks down and increases the likelihood that the allergens can then enter the body and cause and allergic reaction due to interactions with dendritic cells and Th2 cells. The interactions with the dendritic and Th2 cells then cause IgE to have a long lasting binding with mast cells in the skin, lungs and other mucosal areas in the body. I found this finding to be really interesting because the loss of function mutation in the filaggrin gene was only found in the asthmatic people who also had atopic dermatitis but not in the asthmatic people who did not have atopic dermatitis. This finding could help researchers in determining one of the specific pathways that cause children who have high exposure to indoor pollutants to have atopic dermatitis leading to asthma and other respiratory problems.
I agree that it is very interesting that the mutation in the filaggrin gene leads to an increase likelihood to develop both asthma and atopic dermatitis. It makes me wonder how much this gene is of interest in regards to allergic diseases, and how much the protein it codes for plays a role in protecting the body from foreign invaders via the skin. I’m curious what role the protein product of the filaggrin gene plays in skin integrity, and if treatment is available to supplement this loss of integrity. With the increase in gene therapy technologies, the filaggrin gene is certainly of interest in that this target could improve the quality of life for millions of people with asthma and other allergy related diseases, as well as prevent allergies early life and thus the development as age increases.
This is a fascinating discovery. Upon doing some research, I found a study that worked closely in trying to fully sequence the gene FLG that makes the large protein filaggrin. In their overall conclusions, they seemed to be confident about being closer to finding the cure to eczema, a type of dermatitis frequently linked to AD and asthma. Also, with the current knowledge and the correlations with AD that leads to asthma makes it a more interesting subject to explore. It turns out that eczema is a difficult allergy to study because there are not many model organisms that have similar diseases. Still, this lab was able to replicate an FLG gene mutation on mice that were highly analogous to the mutations observed in humans, with elevated IgE and Th2 cytokine responses. A future study their lab aims to research is to figure out a treatment that targets the period of efficacy to prevent eczema — figuring out if the timing when the gene turns on or off can be very helpful in figuring out a cure to eczema. Lastly, does this mean that if they can find a cure to eczema, will this also cure AD and asthma, too, since the common link between both eczema and asthma is AD? I love how science is forever progressive. One question lead to another and eventually leads to cutting-edge discoveries.