Allergies are affecting more people each year and the numbers are not declining anytime soon. Statistics available from the National Institutes of Health suggest that hay fever and other allergic diseases have shot up by 200 to 300 percent in the last 40 years.
It’s even more alarming that over half of today’s Americans will experience an allergy to one thing or the other during their lives.1 Shockingly, around a billion people now suffer from allergic diseases worldwide. Besides outdoor air pollution, even our houses, our bodies and the food we eat contribute to the allergy epidemic.
Lesser Known Causes Of Allergies
1. Climate Change
We all know that the world is getting warmer and the ice caps are melting faster than ever. But what has that got to do with allergies? Environmental conditions that create global warming and climate change is a major cause of allergies.
A study of the pollen levels in the US shows a steady increase in pollen production during this century (from 2001) and predicts that the pollen levels can triple by 2040.2
Increasing pollen levels have a lot to do with the pollution that is causing climate change. Another report attributes greater pollen to higher atmospheric carbon dioxide, which is the result of industrial and automotive pollution.3
Studies suggest that the pollen grains can actually be toxic.4 Pollen grains contain an enzyme that damages the lining of the respiratory tract (nose and lungs), which in turn increases the allergic reactions. Besides increasing the pollen load, pollution makes pollen more allergenic.5
Polluted air causes damage to our respiratory tissues and makes our environment more likely to cause allergies. Research shows that children who are exposed to heavy vehicular traffic are at an increased risk of developing pollen allergy.6
Like any other ailments, pollen allergy impairs their performance at school and affects their sleep. Even adults are vulnerable to this risk as pollen allergy interferes with driving skills and productivity at work.
Formaldehyde is a colorless, flammable gas at room temperature and has a strong odor. Exposure to formaldehyde is known to cause many adverse health effects. This chemical is released into the air in our bedrooms, kitchens, and living rooms from glued wood products, furnishings, and smoke. It is both a powerful irritant and an allergen.
Scientists have established a direct link between the levels of formaldehyde found in homes and the possibility that children in those homes would develop allergies to common inhalants, like pollen and dust. Formaldehyde levels in homes is increasing by the day and resulting in a surge in allergies.7
Triclosan is an antibacterial chemical that is commonly used in personal care products and cleaning solutions. It has been found in the nasal secretions of almost half of the population in the US. Exposure to triclosan can alter the bacteria found in our bodies and increases8 the chances of children developing asthma9 or hay fever.10 In lab experiments on animals, triclosan exposure was shown to increase the possibility of developing a peanut allergy.11
5. Fast Food
Certain foods that we eat also play a key role in causing allergies. An analysis by the International Study of Asthma and Allergies in Children observed that consumption of fast food more than thrice a week increases the risk of allergic diseases in children and adolescents.12 On the other hand, eating fruits at least thrice a week greatly decreases the risk as fruits contain protective nutrients called flavonoids, which are not found in commercial fast foods.
Toxic Environment And Inherited Allergies
Recent research reveals that these environmental factors, which cause allergies can also affect the function of human genes. These changes to the genes, called epigenetic modifications, can be transmitted from the mother to the child for many generations.13
The allergies created today have the potential to affect our future generations and adversely impact human health in the future. This effect has been clearly demonstrated in the well-known familial clustering of allergic diseases, in which maternal allergy are predominant.14
Using Medications To Treat Allergies
Treating or subduing the symptoms of allergies using medications is not a permanent solution. Many studies have found that the commonly used drugs such as antihistamines can lead to a long-term decrease in cognitive function.15 16 More importantly, medication does not prevent the epigenetic effects of the allergy epidemic but only attempts to suppress the symptoms.
|↑1||Hoppin, Jane A., Renee Jaramillo, Paivi Salo, Dale P. Sandler, Stephanie J. London, and Darryl C. Zeldin. “Questionnaire predictors of atopy in a US population sample: findings from the National Health and Nutrition Examination Survey, 2005–2006.” American journal of epidemiology 173, no. 5 (2011): 544-552.|
|↑2||The Year 2040: Double The Pollen, Double The Allergy Suffering? American College of Allergy, Asthma & Immunology. 2012.|
|↑3||Schmidt, Charles W. “Pollen overload: seasonal allergies in a changing climate.” Environmental health perspectives 124, no. 4 (2016): A70.|
|↑4||Dharajiya, Nilesh, Istvan Boldogh, Victor Cardenas, and Sanjiv Sur. “Role of pollen NAD (P) H oxidase in allergic inflammation.” Current opinion in allergy and clinical immunology 8, no. 1 (2008): 57.|
|↑5||Behrendt, H., W. M. Becker, C. Fritzsche, W. Sliwa-Tomczok, J. Tomczok, K. H. Friedrichs, and J. Ring. “Air pollution and allergy: experimental studies on modulation of allergen release from pollen by air pollutants.” International archives of allergy and immunology 113, no. 1-3 (1997): 69-74.|
|↑6||Codispoti, Christopher D., Grace K. LeMasters, Linda Levin, Tiina Reponen, Patrick H. Ryan, Jocelyn M. Biagini Myers, Manuel Villareal et al. “Traffic pollution is associated with early childhood aeroallergen sensitization.” Annals of Allergy, Asthma & Immunology 114, no. 2 (2015): 126-133.|
|↑7||Garrett, M. H., M. A. Hooper, B. M. Hooper, P. R. Rayment, and M. J. Abramson. “Increased risk of allergy in children due to formaldehyde exposure in homes.” Allergy 54, no. 4 (1999): 330-337.|
|↑8||Syed, Adnan K., Sudeshna Ghosh, Nancy G. Love, and Blaise R. Boles. “Triclosan promotes Staphylococcus aureus nasal colonization.” MBio 5, no. 2 (2014): e01015-13.|
|↑9||Spanier, Adam J., Tracy Fausnight, Tareq F. Camacho, and Joseph M. Braun. “The associations of triclosan and paraben exposure with allergen sensitization and wheeze in children.” In Allergy and Asthma Proceedings, vol. 35, no. 6, pp. 475-481. OceanSide Publications, Inc, 2014.|
|↑10||Bertelsen, Randi J., Matthew P. Longnecker, Martinus Løvik, Antonia M. Calafat, K‐H. Carlsen, Stephanie J. London, and K. C. Lødrup Carlsen. “Triclosan exposure and allergic sensitization in Norwegian children.” Allergy 68, no. 1 (2013): 84-91.|
|↑11||Tobar, Steven, Leticia Tordesillas, and M. Cecilia Berin. “Triclosan promotes epicutaneous sensitization to peanut in mice.” Clinical and translational allergy 6, no. 1 (2016): 13.|
|↑12||Reznik, Marina. “Fast Food Linked to Asthma and Allergies in Children.” Science Translational Medicine 5, no. 171 (2013): 171ec26-171ec26.|
|↑13||Lovinsky-Desir, Stephanie, and Rachel L. Miller. “Epigenetics, asthma, and allergic diseases: a review of the latest advancements.” Current allergy and asthma reports 12, no. 3 (2012): 211-220.|
|↑14||Wu, Chih-Chiang, Rong-Fu Chen, and Ho-Chang Kuo. “Different implications of paternal and maternal atopy for perinatal IgE production and asthma development.” Clinical and Developmental Immunology 2012 (2012).|
|↑15||Gray, Shelly L., Melissa L. Anderson, Sascha Dublin, Joseph T. Hanlon, Rebecca Hubbard, Rod Walker, Onchee Yu, Paul K. Crane, and Eric B. Larson. “Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study.” JAMA internal medicine 175, no. 3 (2015): 401-407.|
|↑16||Okamura, Nobuyuki, Kazuhiko Yanai, Makoto Higuchi, Jun Sakai, Ren Iwata, Tatsuo Ido, Hidetada Sasaki, Takehiko Watanabe, and Masatoshi Itoh. “Functional neuroimaging of cognition impaired by a classical antihistamine, d‐chlorpheniramine.” British journal of pharmacology 129, no. 1 (2000): 115-123.|