Schlesinger R B, Chen L C
Department of Environmental Medicine, New York University Medical Center, New York 10016.
Environ Res. 1994 Apr;65(1):69-85. doi: 10.1006/enrs.1994.1022.
Biological responses to inhaled acid sulfates result from the deposition of hydrogen ion (H+) on airway surfaces. Thus, effects from sulfuric acid and ammonium bisulfate, the two major ambient species, have been assumed to be the same for a given H+ concentration within the exposure atmosphere, assuming similar respiratory tract deposition patterns. However, recent inhalation studies have indicated that sulfuric acid is disproportionately potent compared to ammonium bisulfate when the H+ content of the exposure atmosphere is considered, suggesting that some factors following inhalation affect the amount of H+ contacting airway surfaces. This study assessed a mechanism potentially underlying this phenomenon, namely, the extent of neutralization by respiratory tract ammonia. This was evaluated using a physical model system designed to mimic transit of these aerosols in the upper respiratory tract of the animal model used in this laboratory, the rabbit. The results suggest that for equal exposure quantities of H+, more acid would be deposited when sulfuric acid is inhaled than when ammonium bisulfate is inhaled. Furthermore, results from a series of in vitro exposures of tracheal epithelial cells to sulfuric acid and ammonium bisulfate aerosols indicated that the biological response is a function of the total mass (ionic) concentration of H+ deliverable to the cells or the total extractable H+ per particle. The results of this study have possible implications for ambient monitoring of particulate-associated strong acidity, suggesting that it may be necessary to specilate such measures into the relative amounts of H+ as sulfuric acid or ammonium bisulfate in order to most accurately relate atmospheric acid levels to observed health effects. In addition, since much of the ambient particulate-associated H+ exists as sulfuric acid/ammonium bisulfate mixtures rather than pure compounds, H(+)-associated health effects from controlled exposure studies of sulfuric acid may not be transferable to ambient population situations on a 1:1 basis. Since any such errors in exposure assessment will necessarily bias downward the strength of H(+)-related health effects associations found via epidemiological studies, failure to address the specification of H+ may cause such studies to underestimate the human health effects of strong acids.
对吸入酸性硫酸盐的生物反应源于氢离子(H⁺)在气道表面的沉积。因此,假设呼吸道沉积模式相似,对于暴露环境中给定的H⁺浓度,硫酸和硫酸氢铵这两种主要的环境物质的影响被认为是相同的。然而,最近的吸入研究表明,当考虑暴露环境中的H⁺含量时,硫酸比硫酸氢铵的效力要强得多,这表明吸入后某些因素会影响与气道表面接触的H⁺量。本研究评估了这一现象潜在的一种机制,即呼吸道氨的中和程度。使用一个物理模型系统对此进行了评估,该系统旨在模拟这些气溶胶在本实验室所使用的动物模型(兔子)上呼吸道中的传输过程。结果表明,对于等量暴露的H⁺,吸入硫酸时比吸入硫酸氢铵时会有更多的酸沉积。此外,一系列气管上皮细胞体外暴露于硫酸和硫酸氢铵气溶胶的结果表明,生物反应是可递送至细胞的H⁺总质量(离子)浓度或每个颗粒可提取的H⁺总量的函数。本研究结果对与颗粒物相关的强酸度的环境监测可能具有启示意义,这表明可能有必要将此类测量细分为硫酸或硫酸氢铵中H⁺的相对含量,以便最准确地将大气酸度水平与观察到的健康影响联系起来。此外,由于环境中与颗粒物相关的H⁺大多以硫酸/硫酸氢铵混合物而非纯化合物的形式存在,硫酸对照暴露研究中与H⁺相关的健康影响可能无法按1:1的比例直接应用于环境人群情况。由于暴露评估中的任何此类误差必然会使通过流行病学研究发现的与H⁺相关的健康影响关联强度向下偏差,未能考虑H⁺的具体情况可能会导致此类研究低估强酸对人类健康的影响。