[Impact of different temperatures and ambient PM2.5 on the cytotoxicity and cytophagocytic function of alveolar macrophages of rat].

OBJECTIVE: To investigate the interactive effects of different temperatures and ambient PM2.5 on the rat alveolar macrophages. METHODS: The rat alveolar macrophages were collected. The cells were exposed in vitro to 18℃, 24℃, 30℃, 37℃ and 43℃ with PM2.5 at the concentrations of 100 µg/ml, 50 µg/ml, 25 µg/ml and 0 µg/ml respectively. The cells were cultured in the different cases for 8 hours, then cytotoxicity was assessed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide(MTT)reduction assay and phagocytosis function of macrophages was assessed by neutral red absorption test. RESULTS: The relative survival rate and the cytophagocytic function of alveolar macrophages of rats among the different concentration groups decreased significantly (P<0.05) compared with the blank control group. Both were dose-dependent. The 37℃ group had the highest level of relative survival rate and the cytophagocytic function compared with other different temperatures groups. Interactive effect of different temperatures and ambient PM2.5 was not observed. But the lower temperature and the higher PM2.5 concentration group had stronger toxicity to alveolar macrophages. CONCLUSIONS: The results suggested that different temperatures and ambient PM2.5 have cytotoxicity on alveolar macrophages,injuring the phagocytosis. The two factors had some interaction.

Improving Knowledge about Children's Environmental Health in Northwest China.

The main purpose of this study was to identify policy maker opinions and attitudes towards children's environmental health (CEH), potential barriers to child-specific protective legislation and implementation in northwest China, and evaluate knowledge and attitudes about CEH before and after an educational conference. We conducted seventy-two interviews with regional officials, researchers and non-governmental organization representatives from five provinces, and surveyed participants (forty-seven) before and after an educational conference in northwest China about CEH. Interviews identified general consensus among participants of the adverse effects of air pollution on children, yet few participants knew of policies to protect them. Barriers identified included limited funding and enforcement, weak regional governments and absence of child-specific policy-making. After the conference, substantially greater self-efficacy was identified for lead, mercury, air pollution and polychlorinated biphenyls (+0.57-0.72 on a 1-5 Likert scale, p = 0.002-0.013), and the scientific knowledge for the role of environment in children's health (+0.58, p = 0.015), and health care provider control (+0.52, p = 0.025) were rated more strongly. We conclude that policy makers in Northwest China appreciate that children are uniquely vulnerable, though additional regulations are needed to account for that vulnerability. Further research should examine effectiveness of the intervention on a larger scale and scope, and evaluate the usefulness of such interventions in translating research into improved care/reduced exposure to environmental hazards.

Rat lung response to PM2.5 exposure under different cold stresses.

Ambient particulate matters and temperature were reported to have additive effects over the respiratory disease hospital admissions and deaths. The purpose of this study is to discuss the interactive pulmonary toxicities of cold stress and fine particulate matter (PM2.5) exposure by estimating inflammation and oxidative stress responses. 48 Wistar male rats, matched by weight and age, were randomly assigned to six groups, which were treated with cold stress alone (0 °C, 10 °C, and 20 °C (Normal control)) and cold stresses plus PM2.5 exposures respectively. Cold stress alone groups were intratracheal instillation of 0.25 mL normal saline, while cold stress plus PM2.5 exposure groups were intratracheal instillation of 8 mg/0.25 mL PM2.5. These procedures were carried out for three times with an interval of 48 hours for each treatment. All rats were sacrificed after 48 hours of the third treatment. The bronchoalveolar lavage fluid (BALF) was collected for analyzing inflammatory cells and cytokines, and lung homogenate MDA was determined for oxidative stress estimation. Results showed higher level of total cell and neutrophil in the BALF of PM2.5 exposed groups (p < 0.05). Negative relationships between cold stress intensity and the level of tumor necrosis factor alpha (TNF-a), C-reactive protein (CRP) interleukin-6 (IL-6) and interleukin-8 (IL-8) in BALF were indicated in PM2.5 exposure groups. Exposure to cold stress alone caused significant increase of inflammatory cytokines and methane dicarboxylic aldehyde (MDA) and decline of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity only in 0 °C exposure group (p < 0.05). The two-way ANOVA found significant interactive effects between PM2.5 exposure and cold stress in the level of neutrophil, IL-6 and IL-8 and SOD activity (p < 0.05). These data demonstrated that inflammation and oxidative stress involved in the additive effect of PM2.5 exposure and cold stress on pulmonary toxicity, providing explanation for epidemiological studies on the health effect of ambient PM2.5 and cold stress.