Last week, LI suffered from a runny nose, sneezing, fever, and headache. The usual. LI is allergic to something in Austin, as are most people who live in Austin. It is a cyclical thing: for me, October and March are bad times. There�s mold, cedar pollen, ragweed. Supposedly, cedar trees shed pollen when the temperature suddenly changes. I have to navigate with a bloodstream full of whatever is released from the cheap antihistamines I buy into my bloodstream when the temperature suddenly changes. The bitch of this is, the core bitch of this is, that autumn is the prettiest time in Austin. The skies are big and blue, the temperature is mild, the wind picks up in the morning, there�s an ache outside the window that makes you want to not be inside � and then to be sneezing violently throughout this. It seems so grossly unfair.
The Bulletin of the History of Medicine, everybody�s favorite journal, has an article in the Summer issue by Gregg Mitman on how, in the late nineteenth century, allergy sufferers among the upper classes would vacation in allergy free zones, like mountains. Allergy, mountain resorts, and the money to stay in them forms the nexus he examines in Hay Fever Holiday, Health, Leisure and place in Gilded Age America.
We went from Milman�s article, which names John Bostock as the first person to identify hay fever, on a search for information about this Bostock. Bostock rang no bells. So we looked up a Lancet article from 1993, which had some very interesting information about Bostock. Apparently, the kind of catarrhal dysfunction suffered by Bostock was very rare in the early nineteenth century. Bostock came from North England � significantly, one of the early zones of industrialization. The Lancet author uses Bostock, who believed his �summer colds� were temperature related, and another Northern English doctor, Charles Blackley:
�Bostock did not relate his condition to pollen but believed that its seasonal incidence was due to physical factors, possibly temperature. Charles Blackley, a physician in Manchester who also suffered from hay fever, collected some grass pollen in the summer and stored it in a bottle until the middle of the winter. He then removed the top of the bottle and inhaled the pollen. This immediately caused an acute attack with streaming eyes, running nose, and sneezing. This simple and elegant exeriment proved that hay fever was a sensitivity to pollen.
"These historical facts raise the question as to why the first accounts of hay fever and its mechanism came from two physicians from the north-west of England--which was at that time very far removed from the centres of medical excellence and academia such as London, Edinburgh, Paris, and Berlin. To this may be added the question as to why hay fever first appeared at the beginning of the 19th century. The most likely answer to both these questions relates to a third question--was there anything special about the north of England at the beginning of the 19th century? The obvious answer is the Industrial Revolution which began in this area and led to massive chemical pollution for the first time in human history. Chronic chemical damage to the nasal mucosa would facilitate the entry of pollen antigens, leading to immunological sensitisation.
"According to our current understanding hay fever is due to an allergy to pollen in sensitive subjects. The allergic or sensitivity state is manifested by a high IgE which is probably inherited as an autosomal dominant on chromosome 11q.(n8) This explanation does not, however, explain the rarity of the condition before 1800 or its greatly increased prevalence since; grass has been a feature of the landscape for many thousands of years. A genetic mutation leading to a raised IgE could not be the explanation because a mutation in 1800 could not spread to 10% of the population in less than 200 years. This paradox only becomes explicable if chemical pollution is entered into the equation, coincident with the Industrial Revolution in about 1800.
"Work in laboratory animals points to an interaction between allergens and pollutants such as SO2, NO2, O3, and vehicle exhausts. Thus exposure of guineapigs to ozone at 5 parts per million increases the likelihood of sensitisation and anaphylaxis after inhalation of an albumen aerosol.(n10) Intraperitoneal sensitisation of mice to Japanese cedar pollen occurs with concurrent administration of diesel exhaust-particles but not without��
Another fine mess this industrial revolution has gotten us into! Odd, really, that we put up with so much unnecessary misery in this civilization, all for the sake of our petro fix. Sneezers of the world, unite! You have nothing to loose but your prescriptions for stronger anti-histamines! Ratify that Kyoto treaty!