Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA.
Inhal Toxicol. 2011 Nov;23(13):792-804. doi: 10.3109/08958378.2011.609917.
Coal-fired power plant emissions can contribute a significant portion of the ambient air pollution in many parts of the world.
We hypothesized that exposure to simulated downwind coal combustion emissions (SDCCE) may exacerbate pre-existing allergic airway responses.
Mice were sensitized and challenged with ovalbumin (OVA). Parallel groups were sham-sensitized with saline. Mice were exposed 6 h/day for 3 days to air (control, C) or SDCCE containing particulate matter (PM) at low (L; 100 μg/m³), medium (M; 300 μg/m³), or high (H; 1000 μg/m³) concentrations, or to the H level with PM removed by filtration (high-filtered, HF). Immediately after SDCCE exposure, mice received another OVA challenge (pre-OVA protocol). In a second (post-OVA) protocol, mice were similarly sensitized but only challenged to OVA before air/SDCCE. Measurement of airway hyperresponsiveness (AHR), bronchoalveolar lavage (BAL), and blood collection were performed ~24 h after the last exposure.
SDCCE significantly increased BAL macrophages and eosinophils in OVA-sensitized mice from the post-OVA protocol. However, there was no effect of SDCCE on BAL macrophages or eosinophils in OVA-sensitized mice from the pre-OVA protocol. BAL neutrophils were elevated following SDCCE in both protocols in nonsensitized mice. These changes were not altered by filtering out the PM. In the post-OVA protocol, SDCCE decreased OVA-specific IgG₁ in OVA-sensitized mice but increased levels of total IgE, OVA-specific IgE and OVA-specific IgG₁ and IgG(2a) in non-sensitized animals. In the pre-OVA protocol, SDCCE increased OVA-specific IgE in both sensitized and non-sensitized animals. Additionally, BAL IL-4, IL-13, and IFN-γ levels were elevated in sensitized mice.
These results suggest that acute exposure to either the particulate or gaseous phase of SDCCE can exacerbate various features of allergic airway responses depending on the timing of exposure in relation to allergen challenge.
燃煤电厂的排放物可能是世界许多地区环境空气污染的主要来源。
我们假设接触模拟下风煤燃烧排放物（SDCCE）可能会加剧预先存在的过敏性气道反应。
将小鼠致敏并用卵清蛋白（OVA）进行攻毒。平行组用生理盐水进行假致敏。小鼠每天暴露于空气中 6 小时（对照，C）或 SDCCE 中，其中包含颗粒物（PM），浓度分别为低（L；100μg/m³）、中（M；300μg/m³）或高（H；1000μg/m³），或用过滤器去除 PM 后暴露于 H 水平（高过滤，HF）。SDCCE 暴露后，小鼠立即接受另一次 OVA 攻毒（预 OVA 方案）。在第二个（后 OVA）方案中，小鼠以类似方式致敏，但仅在空气/SDCCE 前接受 OVA 攻毒。末次暴露后约 24 小时进行气道高反应性（AHR）、支气管肺泡灌洗（BAL）和血液采集。
SDCCE 显著增加了后 OVA 方案中 OVA 致敏小鼠 BAL 中的巨噬细胞和嗜酸性粒细胞。然而，SDCCE 对前 OVA 方案中 OVA 致敏小鼠的 BAL 巨噬细胞或嗜酸性粒细胞没有影响。非致敏小鼠的 BAL 中性粒细胞在两个方案中均因 SDCCE 而升高。这些变化不会因过滤掉 PM 而改变。在后 OVA 方案中，SDCCE 降低了 OVA 致敏小鼠的 OVA 特异性 IgG₁，但增加了非致敏动物的总 IgE、OVA 特异性 IgE、OVA 特异性 IgG₁ 和 IgG(2a)。在前 OVA 方案中，SDCCE 增加了致敏和非致敏动物的 OVA 特异性 IgE。此外，致敏小鼠的 BALIL-4、IL-13 和 IFN-γ 水平升高。
这些结果表明，急性接触 SDCCE 的颗粒相或气相均可根据过敏原攻毒与暴露的时间关系加剧各种过敏性气道反应特征。
