Acute asthmatic response

Patients who smoke should be strongly encouraged to quit cigarette smoking decreases the efficacy of inhaled corticosteroids and can trigger an acute asthmatic response.3 All patients should also avoid secondhand smoke. Parents of children with asthma should be instructed not to smoke in the home and not to allow others to smoke in the home. Patients should also avoid outdoor activities when air quality is poor and avoid exposure to other irritants such as hairspray, paint, exhaust fumes, and smoke from any fire. 

There are numerous reports on changes in SOD and catalase activities in various diseases [30,41, 97,150], e.g., reduced SOD activity in lung cells (by about 50% in bronchial epithehal cells) was found in asthma and suggested to be a marker of the inflammation characterizing asthma [194]. Loss of SOD occurs within minutes of an acute asthmatic response [195]. 

In another pattern of sensitization response, a worker who has had only minimal upper respiratory symptoms or no apparent effects from several weeks of low-level exposure may suddenly develop an acute asthmatic reaction to the same or a slightly higher level. The asthmatic reaction may be severe, sometimes resulting in status asthmaticus, which may be fatal if exposure continues. ... 

Sauder LR, Green DJ, Chatham MD, et al. 1987. Acute pulmonary response of asthmatics to 3.0 ppm formaldehyde. Toxicol Ind Health 3 569-577. 

Epinephrine usually Is administered slowly by Intravenous (IV) Injection to relieve acute asthmatic attacks not controlled by other treatments. Intravenous Injection produces an Immediate response. Use of EPI with drugs that enhance cardiac arrhythmias (digitalis or quinidine) Is not recommended. Tricyclic antidepressants and MAO Inhibitors will potentiate the effects of EPI on the heart. Epinephrine should be used with caution In Individuals suffering from hyperthyroidism, cardiovascular disease, hypertension, or diabetes. Adverse effects Include palpitations, tachycardia, sweating, nausea and vomiting, respiratory difficulty, dizziness, tremor, apprehension, and anxiety. 

In summary, current information suggests that the mechanism of airway narrowing during the early asthmatic response is an acute bronchoconstrictor response caused mainly by an IgE-dependent immediate hypersensitivity reaction. Of the preformed and newly synthesized mediators released from mast cells during these reactions, the cysteinyl leukotrienes appear to be the most important in the pathogenesis of the EAR. 

The database for HFC-134a is extensive it contains studies with both human subjects and animal models. Potentially sensitive populations, including patients with COPD and adult and pediatric asthmatic patients, were tested with direct inhalation of HFC-134a from metered-dose inhalers. The response of these groups was no different than that of healthy adults. The animal studies covered acute, subchronic, and chronic exposure durations and addressed systemic toxicity as well as neurotoxicity, reproductive and developmental effects, cardiac sensitization, genotoxicity, and carcinogenicity. The metabolism of HFC-134a is well understood, and the relationship of exposure con... 

There is therefore a need to investigate atopy, particularly as that variable may interact with dust exposure, in cotton textile mills." The reader is left with the thought that perhaps "reactors" who exhibit symptoms of acute byssinosis in a cotton mill might be in some sense people who are not obvious asthmatics but who, however, have some minimal or borderline type of asthma or other mildly increased bronchial sensitivity. Merchant et al. (51) tested workshift declines in FEVi workers exposed to cotton dust. In their summary they state "The patterns of FEVi response over a week suggest that there are distinct individual patterns of response not dependent upon previous cotton dust exposure."... 

Regular salbutamol has been compared with salbutamol, taken as needed, in mild asthmatics. There was no change in asthma control nor any increase in the frequency or severity of exacerbation (23). As the bronchodilator response is maintained, patients can be advised to use short-acting beta2-agonists to relieve acute bronchoconstriction and if necessary to increase the dose. 

In one study, the various P2-AR haplotypic combinations (see Section 2. for description and ref. 3 for nomenclature) were utilized to assess the acute response to a standard dose (two puffs) of albuterol, with the change in forced expiratory volume in 1 s (FEVj) as the outcome measure. As shown in Fig. 12, there was a relationship between haplotype pair and FEVj response (p = 0.007 by analysis of covariance). The two homozygous haplotype pairs (2 and 4) were further studied in transient transfected cells, with P2-AR mRNA and protein as measures of expression. Haplotype 4 had approx 50% decreased expression compared to haplotype 2. This was entirely consistent with the physiological data for the asthmatics in that those with the 4/4 haplotype had a lower FEV) response to albuterol compared to those with the 2/2 haplotype. Those with the 4/4 haplotype, then, may be the least responsive to acute administration of P-agonist, and either alternative dosing or different agents might be considered for these individuals. 

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