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J. Examination of the Effects of Certain Acute Environmental Exposures on Future Respiratory Health Consequences
Pages 399-416

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From page 399...
... Low dose inhalation exposure of mustard gas has been noted to result in chest tightness while higher doses have resulted in sneezing, lacrimation, rhinorrhea, nasal bleeding, sore throat, hoarseness and cough.) The WHO has reported the pulmonary effects in Iranian patients exposed during the Iran-Iraq war.2~3 Acute effects included: (2 - hrs)
From page 400...
... In order to evaluate the respiratory health risk associated with repeated brief overexposures at lower levels review of indirect evidence will focus on examining the link between acute and chronic respiratory responses to such agents. One central difficulty in examining this question is the absence of knowledge about the early stages of environmentally related pulmonary diseases coupled with almost no knowledge on the natural (longitudinal)
From page 401...
... These effects were present after controlling for cigarette smoking. In summary, there is clear evidence of acute respiratory effects from chlorine exposures which include both acute bronchitis and airway obstruction as well as inflammatory bronchoconstriction (RADS)
From page 402...
... These include evidence of bronchial constriction and chest tightness.4 Studies of chronic respiratory effects associated with sulfur dioxide exposures have yielded mixed results. However, those which included individual assessment or assignment of SO2 exposure have demonstrated accelerated loss of pulmonary function overall as well as among those with poorer baseline function.~5 ~6 There are, however, some important differences between the two irritants when considering the impact of acute overexposures.
From page 403...
... A follow-up of survivors of a subway fire suggested persistence of small airway damage and respiratory symptoms at six months and two years.26 In 1985 Brooks, et al., described the clinical condition of reactive airways dysfunction syndrome (RADS) .27 The condition is asthma-like but differs from occupational asthma because of an absence of a preceding period for sensitization to occur and the onset of illness after a single overexposure.
From page 404...
... A number of studies, both cross-sectional and longitudinal, have examined the effect of cotton textile employment on pulmonary function. Many of the cross-sectional studies have shown lower function in cotton workers,33 39 48 49 50 but inconsistent findings have been reported for the relationship of the lower function to duration of employment35 36 and current dust exposures.33 48 One study did show a relationship to a dust index.32 The longitudinal studies have consistently shown greater loss of FEW among cotton textile workers 22~36 38 42,5i In only one of those with under three years follow-up was an association of function loss with duration noted.9 In the three with five or more years, despite methodologic flaws there was not only lower function in the cotton workers but
From page 405...
... Isocyanates These reactive chemical agents have been reported to cause a wide range of nonmalignant respiratory health effects although there are substantial differences in the proportion of the population at risk for each.55 In 1951, case reports of isocyanate-related pulmonary effects called attention to a new occupational asthma.56 Sensitization was reported to occur as early as after only one high exposure,57 but onset could also be delayed for a number of years after first exposure.58 59 Unlike with high molecular weight agents which cause occupational asthma, however, further study of isocyanate asthma cases showed that measurable IgE and airway hyperreactivity was not invariably an essential feature.55 60 6i The course of isocyanate asthma includes the fact that as many as half of seriously affected workers who leave work do not recover.62 63 64 Although it was not initially expected, continued investigation of the effects of work exposure to isocyanates revealed evidence of a number of respiratory effects other than asthma which were important and a series of epidemiologic studies ensued. There is good evidence that high levels of exposure are associated with chemical bronchitis65 and, recently, with reactive airway dysfunction syndrome.66 Independent of asthma or acute response to serious overexposures,
From page 406...
... There is also evidence that the acute effects are related to the chronic effects both as asthma that does not remit and as cross-shift loss which is related to the rate of subsequent annual loss. Finally, there is evidence that short-term exposures can cause acute responses that are irreversible and progressive, but there is no evidence, either way, as to whether short-term exposures without acute response result in irreversible respiratory effects.
From page 407...
... have been associated with increased respiratory symptoms and decreased vital capacity.79 THE FUNDAMENTAL QUESTION Narrowly Structured For an acute exposure (intense but over only a short interval) to have a causal association with subsequent respiratory disease conditions, must the exposure cause acute irreversible and progressive damage evidence by acute clinical illness or, at minimum, objective changes in lung parameters or severe subjective symptoms?
From page 408...
... , inflammatory bronchoconstriction (acquired airway hyperresponsiveness from nonimmunogenic irritant exposures characterized by reversible airflow obstruction and nonspecific airway hypersensitivity) , and pharmacologic bronchoconstriction (reversible airflow limitation without evidence of a hypersensitive subgroup of the population of exposed)
From page 409...
... Inflammatory Bronchoconstriction J Immunologically active substances can cause occupational asthma in some exposed workers while exposure to nonimmunogenic substances (i.e., irritants) may cause reactive airway dysfunction (RADS)
From page 410...
... Although nonspecific bronchial reactivity is often noted in the majority of patients with occupational asthma, it is not known whether this is a result of the exposure or a predisposing factor. Studies in red cedar asthma suggest that the increased bronchial reactivity is reduced or returns to normal after exposure ceases, suggesting that the reactivity change is a result of the exposure.80 Similar conclusions might be drawn from a recent study comparing subjects responding to cotton dust (with both byssinotic and non-byssinotic symptoms)
From page 411...
... In making the selection, agents were included which are commonly considered primarily as acute respiratory irritants, those known to induce extrinsic asthma, those which are related to non-immunogenic bronchial hyperreactivity, those which are most often responsible for slowly developing chronic fibrosis or granulomatous disease, and one which is believed to cause pharmacologic bronchoconstriction. The chronic respiratory effects associated with each of the agents reviewed included several of the general types of chronic respiratory response rather than being limited to only one type of reaction.
From page 412...
... This may be the most important question to ask and, unforhunately, the one for which no direct evidence could be found. The indirect evidence reported, however, would suggest that it would have to be an unusual disease model which would need to be invoked that could exclude the possible mechanism of change in individual risk factors so that the absence of an acute reaction would elilT~inate the possibility of a chronic effect related to the acute exposure.
From page 413...
... Late evaluation of pulmonary function after acute exposure to chlorine gas. Am Rev Respir Dis (1969)
From page 414...
... Increases in airway responsiveness following acute exposure to respiratory irritants: reactive airway dysfunction syndrome or occupational asthma? Chest (1988)
From page 415...
... The pattern of lung function abnormalities in cotton textile workers. Am Rev Respir Dis (1984)
From page 416...
... Respiratory symptoms and skin sensitivity in workers exposed to proteolytic enzymes in detergent industry. Am Rev Respir Dis (1971)


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