重庆市主要交通干道机动车尾气污染状况

目的：探讨重庆市机动车尾气污染状况,为研究其对人群健康的影响提供依据.方法：测定重庆市主要交通干道空气中铅含量、苯并（a）芘[B（a）P]浓度、总悬浮颗粒、PM10、PM2.5和PM1浓度并进行相关分析.结果：重庆市各主要交通干道尾气污染物浓度均超过国家环境卫生标准.结论：该市应采取措施控制机动车尾气污染环境.     

Respiratory exposure to diesel exhaust particles decreases the spleen IgM response to a T cell-dependent antigen in female B6C3F1 mice.

We investigated the systemic immunotoxic potential of respiratory exposure to diesel exhaust particles (DEP) in this study. Female B6C3F1 mice (approximately 8 weeks old) were exposed to increasing concentrations of DEP intratracheally, 3 times every two weeks, and sacrificed 2 or 4 weeks after the first exposure. The systemic toxicity and immune status in mice were evaluated. Mice exposed to DEP (1 to 15 mg/kg) showed no significant changes in body, spleen, or liver weights. Lung weights were increased in the mice exposed to 15 mg/kg DEP for 2 or 4 weeks. Except for a decreased platelet count, no significant alterations occurred in hematological parameters following DEP exposure. The number of splenic anti-sheep red blood cell (sRBC) IgM antibody-forming cells (AFC) decreased following DEP exposure for 2 weeks. This effect was less severe following 4 weeks of exposure and was only evident in the high dose group. Exposure to DEP also resulted in a significant decrease in the absolute numbers and the percentages of total spleen cells for total, CD4(+), and CD8(+) T cells, while the numbers of B cells and total nucleated cells in spleen were not significantly changed. The proliferative response of splenocytes to the T-cell mitogen, concanavalin A (ConA), as well as their production of IL-2 and IFN-gamma, was decreased dose-dependently following exposure of mice to DEP for 2 weeks, whereas proliferation was not changed in response to anti-CD3 monoclonal antibody. In summary, short-term respiratory exposure of mice to DEP resulted in systemic immunosuppression with evidence of T cell-mediated and possibly macrophage-mediated mechanisms.     

用示踪气体法评价和优选吸气罩

目的 在粉尘发生源处设置适用的局部吸气罩,可以有效地控制粉尘向周围扩散,是预防尘肺病发生的有效措施。为了提供适宜吸气罩的设计,使用了示踪气体法评价吸气罩的效率,对吸气罩的设计进行优选,以提高捕集效率和降低能耗。方法 建立示踪气体评价吸气罩效率的实验风道和方法,采用人工煤气作为示踪气体。结果 实验了长方形和无延伸挡板及有特殊延伸挡板的条缝形吸气罩在不同罩口风速下对示踪气体的捕集效率。导出了捕集效率和距离的关系方程式。实验结果表明:(1)吸气罩与污染源的距离和罩口风速对捕集效率有明显的影响。当罩口风速一定时。吸气罩越靠近污染源,捕集效率越高;而在同一距离上,罩口风速越大,捕集效率就越高。(2)有延伸挡板的条缝形吸气罩的捕集效率高于无延伸挡板条缝形吸气罩,前者采用较低的罩口风速(抽风量)可以得到相应的高捕集效率。结论 使用示踪气体对吸气罩进行优选的结果表明,通过改进吸气罩的形式可以降低所需风量并达到要求的效率,从而为减少通风设施的费用提供了一种重要途径。     

Sustained effect of inhaled diesel exhaust particles on T-lymphocyte-mediated immune responses against Listeria monocytogenes.

Studies have shown that exposure to diesel exhaust particles (DEP) suppresses pulmonary host defense against bacterial infection. The present study was carried out to characterize whether DEP exposure exerts a sustained effect in which inhaled DEP increase the susceptibility of the lung to bacterial infection occurring at a later time. Brown Norway rats were exposed to filtered air or DEP by inhalation at a dose of 21.2 +/- 2.3 mg/m3, 4 h/day for 5 days, and intratracheally instilled with saline or 100,000 Listeria monocytogenes (Listeria) 7 days after the final DEP exposure. Bacterial growth and cellular responses to DEP and Listeria exposures were examined at 3 and 7 days post-infection. The results showed that inhaled DEP prolonged the growth of bacteria, administered 7 days post DEP exposure, in the lung as compared to the air-exposed controls. Pulmonary responses to Listeria infection were characterized by increased production of interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, IL-12, and IL-10 by alveolar macrophages (AM) and increased presence of T lymphocytes and their CD4+ and CD8+ subsets in lung draining lymph nodes that secreted elevated levels of IL-2, IL-6, IL-10, and interferon (IFN)-gamma. Diesel exhaust particles were found to inhibit Listeria-induced production of IL-1beta and TNF-alpha, which are responsible for the innate immunity, and IL-12, which initiates the development of T helper (Th)1 responses, but enhance Listeria-induced AM production of IL-10, which prolongs Listeria survival in these phagocytes. The dual action of DEP on AM production of IL-12 and IL-10 correlated with an inhibition of the development of bacteria-specific T lymphocytes by DEP. Cytokine production by lymphocytes from DEP- and Listeria-exposed rats showed a marked decrease in the production of IL-2, IL-10, and IFN-gamma compared to Listeria infection alone, suggesting either that DEP inhibit the production of cytokines by lymphocytes or that these lymphocytes contained T-cell subsets that are different from those of Listeria infection alone and less effective in mediating Th1 immune responses. This study demonstrates that inhaled DEP, after a 7-day resting period, increase the susceptibility of the lung to bacterial infection occurring at a later time by inhibiting macrophage immune function and suppressing the development of T-cell-mediated immune responses. The results support the epidemiological observations that exposure to DEP may be responsible for the pulmonary health effects on humans.     

Exposure of brown Norway rats to diesel exhaust particles prior to ovalbumin (OVA) sensitization elicits IgE adjuvant activity but attenuates OVA-induced airway inflammation.

Exposure to diesel exhaust particles (DEP) during the sensitization process has been shown to increase antigen-specific IgE production and aggravate allergic airway inflammation in human and animal models. In this study, we evaluated the effect of short-term DEP exposure on ovalbumin (OVA)-mediated responses using a post-sensitization model. Brown Norway rats were first exposed to filtered air or DEP (20.6 +/- 2.7 mg/m3) for 4 h/day for five consecutive days. One day after the final air or DEP exposure (day 1), rats were sensitized with aerosolized OVA (40.5 +/- 6.3 mg/m3), and then again on days 8 and 15, challenged with OVA on day 29, and sacrificed on days 9 or 30, 24 h after the second OVA exposure or the final OVA challenge, respectively. Control animals received aerosolized saline instead of OVA. DEP were shown to elicit an adjuvant effect on the production of antigen-specific IgE and IgG on day 30. At both time points, no significant airway inflammatory responses and lung injury were found for DEP exposure alone. However, the OVA-induced inflammatory cell infiltration, acellular lactate dehydrogenase activity and albumin content in bronchoalveolar lavage (BAL) fluid, and numbers of T cells and their CD4+ and CD8+ subsets in lung-draining lymph nodes were markedly reduced by DEP on day 30 compared with the air-plus-OVA exposure group. The OVA-induced nitric oxide (NO) in the BAL fluid and production of NO, interleukin (IL)-10, and IL-12 by alveolar macrophages (AM) were also significantly lowered by DEP on day 30 as well as day 9. DEP or OVA alone decreased intracellular glutathione (GSH) in AM and lymphocytes on days 9 and 30. The combined DEP and OVA exposure resulted in further depletion of GSH in both cell types. These results show that short-term DEP exposure prior to sensitization had a delayed effect on enhancement of the sensitization in terms of allergen-specific IgE and IgG production, but caused an attenuation of the allergen-induced airway inflammatory responses.     

Exposure to total particulate matter obtained from combustion of diesel vehicles (EURO 3 and EURO 5): Effects on the respiratory systems of emphysematous mice

Air pollution has association with chronic obstructive pulmonary disease (COPD) and reduced life expectancy. This study investigated the deleterious effects caused by tobacco smoke and diesel exhaust particles (DEP) from vehicles operating under EURO 3 and EURO 5 standards. Experiments were carried out on C57BL/6 mice divided into six groups: control group, group exposed to cigarette smoke (CS), two groups exposed to DEP (AAE3 and AAE5), and two groups exposed to tobacco smoke and vehicle DEP (CSE3 and CSE5). Results showed that, when compared to AA, groups AAE3 and AAE5 showed changes in respiratory mechanics, and that DEP originating from EURO 5 diesel vehicles was less harmful when compared to DEP originating from EURO 3 diesel vehicles. Analyses of groups CSE3 and CSE5 revealed increased inspiratory capacity and decreased tissue elastance, when compared to their respective controls, suggesting an exacerbation of changes in respiratory system mechanics compatible with COPD development.     

Physiological and inflammatory responses in an anthropomorphically relevant model of acute diesel exhaust particle exposure are sex and dose-dependent

Context: Diesel exhaust particles (DEP) are an important contributor to suspended particulate matter (PM) in urban areas. While epidemiological evidence exists for a sex-influenced dose-response relationship between acute PM exposure and respiratory health, similar data are lacking for DEP. Further, experimental evidence showing deleterious effects on respiratory health due to acute DEP exposure is sparse.

Objective: To establish and characterize a mouse model of acute DEP exposure, comparing male and female mice and assessing the kinetics of the elemental carbon content of alveolar macrophages (AMs) to relate our model to human exposure.

Materials and Methods: Adult BALB/c mice were intranasally inoculated with 0 (control), 10, 30 or 100 µg DEP in saline. Bronchoalveolar lavage cellular inflammation and cytokine levels were assessed 3, 6, 12, 24, 48 and 168 hours post exposure. Elemental carbon uptake by AMs was additionally assessed at 336 and 672 hours post DEP exposure. Thoracic gas volume and lung mechanics were measured 6 and 24 hours post exposure. Results: DEP resulted in dose-dependent cellular inflammation and cytokine production in both sexes. Males and females responded differently with females having more severe and prolonged neutrophilia, monocyte chemoattractant protein-1 and developing greater abnormalities in lung function. The sexual dimorphism in response was not related to the capacity of AMs to phagocytise DEP.

Conclusions: Our mouse model of acute diesel exhaust particle exposure shows a dose dependency and sexual dimorphism in response. Quantification of elemental carbon in AMs allows for comparison of the results of our study with human studies.     

Occupational exposure to diesel engine exhaust and serum cytokine levels

The International Agency for Research on Cancer has classified diesel engine exhaust (DEE) as a human lung carcinogen. Given that inflammation is suspected to be an important underlying mechanism of lung carcinogenesis, we evaluated the relationship between DEE exposure and the inflammatory response using data from a cross‐sectional molecular epidemiology study of 41 diesel engine testing workers and 46 unexposed controls. Repeated personal exposure measurements of PM_2.5 and other DEE constituents were taken for the diesel engine testing workers before blood collection. Serum levels of six inflammatory biomarkers including interleukin (IL)‐1, IL‐6, IL‐8, tumor necrosis factor (TNF)‐α, macrophage inflammatory protein (MIP)‐1β, and monocyte chemotactic protein (MCP)‐1 were analyzed in all subjects. Compared to unexposed controls, concentrations of MIP‐1β were significantly reduced by ～37% in DEE exposed workers (P < 0.001) and showed a strong decreasing trend with increasing PM_2.5 concentrations in all subjects (P_trend < 0.001) as well as in exposed subjects only (P_trend = 0.001). Levels of IL‐8 and MIP‐1β were significantly lower in workers in the highest exposure tertile of PM_2.5 (>397 µg/m³) compared to unexposed controls. Further, significant inverse exposure‐response relationships for IL‐8 and MCP‐1 were also found in relation to increasing PM_2.5 levels among the DEE exposed workers. Given that IL‐8, MIP‐1β, and MCP‐1 are chemokines that play important roles in recruitment of immunocompetent cells for immune defense and tumor cell clearance, the observed lower levels of these markers with increasing PM_2.5 exposure may provide insight into the mechanism by which DEE promotes lung cancer. Environ. Mol. Mutagen. 59:144–150, 2018. © 2017 Wiley Periodicals, Inc.     

Health effects of soy-biodiesel emissions: bioassay-directed fractionation for mutagenicity

Abstract

Context: Soy biodiesel is the predominant biodiesel in the USA, but there is little understanding of the classes of chemicals responsible for the mutagenicity of its emissions.

Objective: We determined some of the chemical classes responsible for the mutagenicity of the particulate matter (PM) of the emissions from petroleum diesel (B0) and biodiesel containing increasing concentrations of soy methyl esters (B20, B50, and B100).

Materials and methods: We subjected organic extracts of the PM to bioassay-directed fractionation by sequential elution on silica gel with solvents of increasing polarity to produce four fractions per fuel. We injected these onto high performance liquid chromatography to produce 62 sub-fractions per fraction based on chemical polarity and evaluated all fractions and sub-fractions for mutagenicity in Salmonella. We correlated the results with the concentrations of 32 polycyclic aromatic hydrocarbons (PAHs) in the fractions.

Results: The mutagenicity-emission factors of the fractions generally decreased with increasing concentrations of soy in the fuel. Despite the different chemical compositions of the fuels, the extractable organics of all four emissions had similar features: ～60% of the mass was nonpolar, non-mutagenic compounds; most of the PAHs were polar; and most of the mutagenicity was due to weakly polar and polar compounds. Some of the mutagenicity of B20 was due to highly polar compounds.

Conclusions: The PM from soy biodiesel emissions was less mutagenic than that from petroleum diesel, and this reduction was associated with reduced concentrations of various weakly polar, polar, and highly polar mutagens, including PAHs, aromatic amines, nitroarenes, and oxy-PAHs.