Asthma epidemiology

Matricardi, P.M., et al. (2000). Exposure to foodborne and orofecal microbes versus airborne viruses in relation to atopy and allergic asthma, epidemiological study, B.M.J., 320, 412-417. 

Sears MR, Taylor DR. The beta 2-agonist controversy. Observations, explanations and relationship to asthma epidemiology. Drug Saf 1994 ll(4) 259-83. 

However, Pearce et al. [14(NC)] have written that the problem of information bias is of particular concern in asthma epidemiology issues because of the difficulties in defining and measuring asthma, allergic rhinoconjunctivitis and atopic eczema, and the difficulties in obtaining exposure information in the aetiologically relevant time period. However, provided that the information has been collected in a standardized manner, then misclassification will be non-differential, and any bias it produces will usually be towards the null value. 

Pearce N, Beasley R, Burgess C, Crane J Asthma Epidemiology Principles and Methods. New York, Oxford University Press, 1998. 

Myers TR Pediatrics asthma epidemiology Incidence, morbidity and mortality. Respir Care Clin N Am 2000 6 1-14. 

Aggarwal AN, Chaudhry K, Chhabra SK, D Souza GA, Gupta D, Jindal SK, Katiyar SK, Kumar R, Shah B, X jayan VK Asthma Epidemiology Study Group (2006) Prevalence and risk factors for bronchial asthma in Indian adults a multicentie study. Indian J Chest Dis Allied Sd 48(1) 13-22... 

Epidemiological studies of nickel-producing and nickel-using workers seldom indicate excess mortaUty from nonmalignant respiratory disease. Evidence for such effects exists mainly as a few reports of isolated incidents of asthma, pulmonary fibrosis, chronic bronchitis, and emphysema in nickel workers. Nickel may or may not play a causal role in these incidents (131). 

Cobalt compounds can be classified as relatively nontoxic (33). There have been few health problems associated with workplace exposure to cobalt. The primary workplace problems from cobalt exposure are fibrosis, also known as hard metal disease (34,35), asthma, and dermatitis (36). Finely powdered cobalt can cause siUcosis. There is Htfle evidence to suggest that cobalt is a carcinogen in animals and no epidemiological evidence of carcinogenesis in humans. The LD q (rat) for cobalt powder is 1500 mg/kg. The oral LD q (rat) for cobalt(II) acetate, chloride, nitrate, oxide, and sulfate are 194, 133, 198, 1700, 5000, and 279 mg/kg, respectively the intraperitoneal LD q (rat) for cobalt(III) oxide is 5000 mg/kg (37). 

Yang MS, Lee SH, Kim TW, et al Epidemiologic and clinical features of anaphylaxis in Korea. Ann Allergy Asthma Immunol 2008 100 31-36. 

Siroux V. Curt F. Oryszczyn MP, Maccario J, Kauff-mann F Role of gender and hormone-related events on IgE. atopy, and eosinophils in the Epidemiological Study on the Genetics and Environment of Asthma, dO bronchial hyperresponsiveness and atopy. J Allergy Clin Immunol 2004 114 491-498. 

Efforts to incorporate SNP studies into environmental/occupational epidemiology investigations have focused on examining hypothesis-driven associations between exposures and specific polymorphisms. Most common human diseases such as asthma,... 

Schweigert, M.K., Mackenzie, D.P., and Sarlo, K., Occupational asthma and allergy associated with the use of enzymes in the detergent industry a review of the epidemiology, toxicology and methods of prevention, Clin Exp Allergy, 30, 1511, 2000. 

Asthma rates in children in Southern California are high and oxidant pollution levels are likewise high. It is important to determine the relationship between the two. It is also important to determine whether there are chronic pulmonary effects produced by either these oxidants and/or particulate pollution. Since children spend more time outdoors than adults and since they exercise more while outdoors, the added assault from increased ventilation may be of importance. The studies feature a comprehensive exposure assessment that has led to a better understanding of the relationship between exposure and effects. It is also important to identify sub-populations of children and adults who are more susceptible to air pollution-related respiratory effects if they exist. Altered susceptibility could be based on genetic or non-genetic mechanisms (nutritional status for example). Both the epidemiologic and chamber studies provide opportunities to examine issues of hypersusceptibility and to determine the reasons for it if it exists. 

Improved disease reporting, surveillance, and epidemiologic studies of these diseases are needed. Little information exists about either the chronic effects of acute exposure to these marine toxins or about the long-term effects of chronic exposures, e.g., elderly populations in coastal retirement communities experiencing annual HABs. Little information is available about the environmental health effects, e.g., asthma exacerbations, from exposure to these toxins. 

Kemp, T., Pearce, N., Fitzharris, P., et al. (1997) Is infant immunization a risk factor for childhood asthma or allergy Epidemiology. 8, 678-680. 

Limited epidemiological data suggest that chronic human inhalation exposure to kerosene vapor and/or kerosene combustion products from cooking with kerosene stoves does not induce asthmatic respiratory effects. The presence of kerosene stoves in the homes of Malaysian children was not associated with chronic cough, persistent wheeze, asthma, or chest illness (Azizi and Henry 1991). Asthmatic bronchitis and frequent common colds in 3-year-old Japanese children were not associated with the presence of kerosene stoves in their homes (Tominaga and Itoh 1985). The latter study corrected for exposure to passive smoke. These data are of limited usefulness because the duration of exposure was not reported and the levels of kerosene exposure could not be quantified. Finally, it cannot be determined whether actual exposure to kerosene occurred in these individuals because kerosene exposure was assumed to occur if kerosene was used during cooking or if a kerosene stove was present in the home. 

Lugogo NL, Kraft M. Epidemiology of asthma. Clin Chest Med 2006 27 1-15. 

A few epidemiological studies suggest that the overuse of p-adrenoceptor agonists is associated with an overall deterioration in disease control and a slight increase in asthma mortality. This apparent trend may be caused by several factors, the most likely of which is that patients rely too heavily on bronchodilator therapy to control acute symptoms at the expense of antiinflammatory therapy to control the underlying disease process. 

Pearce N, Douwes J (2006) The global epidemiology of asthma in children. Int J Tuberc Lung Dis 10(2) 125-132... 

Pless-Mulloli, T., Howel, D. Prince, H. 2001. Prevalence of asthma and other respiratory symptoms in children living near and away from opencast coal mining sites. International Journal of Epidemiology, 30, 556-563. 

Schoenwetter WF. 2000. Allergic rhinitis Epidemiology and natural history. Allergy Asthma Proc. 21 1-6. 

Pattemore PK, Johnston SL, Bardin PG Virus as precipitants of asthma symptoms. I. Epidemiology. Clin Exp Allergy 1992 22 325-336. 

The large body of epidemiological studies have clearly shown that allergic rhinitis and asthma are frequent diseases, and that both diseases obviously still increase in prevalence [4, 5]. However, without any doubt, there is a direct link between rhinitis and asthma. Several studies in a large number of patients have clearly shown that rhinitis sufferers have a 3- to 7-fold increased risk to also develop asthma within 7 years compared to normal controls. Most of this development actually lies in the early years of childhood, as was recently shown in the MAS and PAT studies [6, 7], In the first study, 5-year-old children sensitized to pollen with allergic rhinitis symptoms developed asthma within 2 years... 

Sulfur mustards (designated H [mustard], HD [distilled mustard], and HT [HD and T mixture]) do not present acute lethal hazards. Their principal effect is severe blistering of the skin and mucous membranes. Epidemiological evidence indicates a causal relationship between exposure to mustard agent at high concentrations and the development of chronic nonreversible respiratory disorders, such as chronic bronchitis and asthma, and ocular diseases, such as delayed recurrent keratitis and prolonged, intractable conjunctivitis (IOM, 1993). Sulfur mustard has been classified as a known human carcinogen based on evidence of in-... 

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