The impact of chronic exposure to air pollution and outcomes in the acute respiratory distress syndrome (ARDS) is unknown. The Nationwide Inpatient Sample (NIS) from 2011 was utilized for this analysis. The NIS is a national database that captures 20% of all US in-patient hospitalizations from 47 states. Patients with ARDS who underwent mechanical ventilation from the highest 15 ozone pollution cities were compared with the rest of the country. Secondary analyses assessed outcomes of ARDS patients for ozone pollution and particulate matter pollution on a continuous scale by county of residence. A total of 8,023,590 hospital admissions from the 2011 NIS sample were analyzed. There were 93,950 patients who underwent mechanical ventilation for ARDS included in the study. Patients treated in high ozone regions had significantly higher unadjusted hospital mortality (34.9% versus 30.8%, p < 0.01) than patients in cities with control levels of ozone. After controlling for all variables in the model, treatment in a hospital located in a high ozone pollution area was associated with an increased odds of in-hospital mortality (OR 1.11, 95% CI 1.08–1.15, p < 0.01). After adjustment for all variables in the model, for each increase in ozone exposure by 0.01 ppm the OR for death was 1.07 (95% CI 1.06–1.08, p < 0.01). Similarly, for each increase in particulate matter exposure by 10 μg/m³, the OR for death was 1.08 (95% CI 1.02–1.16, p < 0.01).Chronic exposure to both ozone and particulate matter pollution is associated with higher rates of mortality in ARDS. These preliminary findings need to be confirmed by further detailed studies.

Cold weather was estimated to account for more than half of weather-related deaths in the U.S. during 2006–2010. Studies have shown that cold-related excessive mortality is especially relevant with decreasing latitude or in regions with mild winter. However, only limited studies have been conducted in the southern U.S. The purpose of our study is to examine impacts of cold weather on mortality in 12 major Texas Metropolitan Areas (MSAs) for the 22-year period, 1990–2011. Our study used a two-stage approach to examine the cold-mortality association. We first applied distributed lag non-linear models (DLNM) to 12 major MSAs to estimate cold effects for each area. A random effects meta-analysis was then used to estimate pooled effects. Age-stratified and cause-specific mortalities were modeled separately for each MSA. Most of the MSAs were associated with an increased risk in mortality ranging from 0.1% to 5.0% with a 1 °C decrease in temperature below the cold thresholds. Higher increased mortality risks were generally observed in MSAs with higher average daily mean temperatures and lower latitudes. Pooled effect estimate was 1.58% (95% Confidence Interval (CI) [0.81, 2.37]) increase in all-cause mortality risk with a 1 °C decrease in temperature. Cold wave effects in Texas were also examined, and several MSAs along the Texas Gulf Coast showed statistically significant cold wave-mortality associations. Effects of cold on all-cause mortality were highest among people over 75 years old (1.86%, 95% CI [1.09, 2.63]). Pooled estimates for cause-specific mortality were strongest in myocardial infarction (4.30%, 95% CI [1.18, 7.51]), followed by respiratory diseases (3.17%, 95% CI [0.26, 6.17]) and ischemic heart diseases (2.54%, 95% CI [1.08, 4.02]). In conclusion, cold weather generally increases mortality risk significantly in Texas, and the cold effects vary with MSAs, age groups, and cause-specific deaths.

In this study, the phototoxicity of cadmium sulfide (CdS), molybdenum disulfide (MoS2), and tungsten disulfide (WS2) nanoparticles (NPs) toward Escherichia coli (E. coli) under UV irradiation (365 nm) was investigated. At the same mass concentration of NPs, the toxicity of three NPs decreased in the order of CdS > MoS2 > WS2. For example, the death rates of E. coli exposed to 50 mg/L CdS, MoS2, and WS2 were 96.7%, 38.5%, and 31.2%, respectively. Transmission electron microscope and laser scanning confocal microscope images of E. coli exposed to three NPs showed the damage of cell walls and release of intracellular components. The CdS-treated cell wall was more extensively damaged than those of MoS2-treated and WS2-treated bacteria. WS2 and MoS2 generated superoxide radical (O2⁻), singlet oxygen (¹O2), and hydroxyl radical under UV irradiation, CdS produced only O2⁻ and ¹O2. CdS and WS2 released ions under UV irradiation, while MoS2 did not. Reactive oxygen species (ROS) generation and toxic ion release jointly resulted in the antibacterial activities of CdS and WS2. ROS generation was the dominant toxic mechanism of MoS2 toward the bacteria. This study highlighted the importance of considering the hazardous effect of sulfide NPs after their release into natural waters under light irradiation condition.

Both carbon nanotubes (CNTs) and perfluorooctane sulfonate (PFOS) are used widely. There is considerable concern regarding their ecotoxicity. CNTs might interact with PFOS in water and result in different impacts compared with those after single exposures. To our knowledge, the developmental toxicity of PFOS in the presence of multi-walled carbon nanotubes (MWCNTs) in the early life stage of zebrafish (from 3 h post fertilization (hpf) to 96 hpf) was investigated for the first time in this study. The embryos and larvae were exposed to PFOS (0.2, 0.4, 0.8, and 1.6 mg/L), MWCNTs (50 mg/L), and a mixture of both. Compared with PFOS exposure, the adverse effects induced by PFOS on the hatching rate of zebrafish embryos and the heart rate and body length of zebrafish larvae were reduced in the presence of MWCNTs, and mortality and malformation were also alleviated. In addition, zebrafish larvae exposed to PFOS showed decreased activities of superoxide dismutase, catalase, and glutathione peroxidase, as well as decreased levels of reactive oxygen species and malondialdehyde, in the presence of MWCNTs, indicating that oxidative stress and lipid peroxidation was relieved. Thus, the presence of MWCNTs reduces the developmental toxicity of PFOS in the early life stage of zebrafish.

Ambient air pollution ranks high among the risk factors that increase the global burden of disease. Previous studies focused on assessing mortality risk and were sparsely performed in populous developing countries with deteriorating environments. We conducted a time-series study to evaluate the air pollution-associated years of life lost (YLL) and mortality risk and to identify potential modifiers relating to the season and demographic characteristics. Using linear (for YLL) and Poisson (for mortality) regression models and controlling for time-varying factors, we found that an interquartile range (IQR) increase in a three-day average cumulative (lag 0–2 day) concentrations of PM2.5, PM10, NO2 and SO2 corresponded to increases in YLL of 12.09 (95% confidence interval [CI]: 2.98–21.20), 13.69 (95% CI: 3.32–24.07), 26.95 (95% CI: 13.99–39.91) and 24.39 (95% CI: 8.62–40.15) years, respectively, and to percent increases in mortality of 1.34% (95% CI: 0.67–2.01%), 1.56% (95% CI: 0.80–2.33%), 3.36% (95% CI: 2.39–4.33%) and 2.39% (95% CI: 1.24–3.55%), respectively. Among the specific causes of death, cardiovascular and respiratory diseases were positively associated with gaseous pollutants (NO2 and SO2), and diabetes was positively correlated with NO2 (in terms of the mortality risk). The effects of air pollutants were more pronounced in the cool season than in the warm season. The elderly (>65 years) and females were more vulnerable to air pollution. Studying effect estimates and their modifications by using YLL to detect premature death should support implementing health risk assessments, identifying susceptible groups and guiding policy-making and resource allocation according to specific local conditions.

Exposure to particulate matter with diameter ≤10 μm (PM10) entails well documented adverse effects on human health. In the last decade, concentration of PM10 in Lombardy (10 million inhabitants), Italy, has been gradually decreasing. We evaluated how the mortality burden due to PM10 varied in that same period.We focused on 13 areas of the Region in 2003–2014: 11 cities with more than 50,000 inhabitants, 1 smaller alpine town and 1 agricultural province. For each area, we collected PM10 annual average concentrations and natural mortality data, and we used the posterior area-specific effects from a previous Bayesian meta-analysis to estimate the short-term impact of PM10 on mortality, in terms of deaths attributable (AD) to annual average exposures exceeding the WHO threshold of 20 μg/m3.PM10 annual average values showed a non-homogenous decreasing trend in the investigated time period in most of the areas. Overall, the population-weighted exposure levels decreased, except for a peak in 2011, but never met the WHO threshold. In 2003–2006, PM10 levels were responsible, on average, for 343.0 annual AD from natural causes that decreased to 253.5 in 2007–2010 and to 208.3 in 2011–2014. Overall we estimated that PM10 was responsible for about 1% of all natural deaths (min-max range: 0.86%–1.42%); the impact was heterogeneous among areas.By collecting routinely available data for the most populated areas in Lombardy, we returned a picture of air pollution and health trends in the last decade. Notwithstanding the observed reduction in PM10 between 2003 and 2014 and the resulting decline in the number of AD, the impact is still relevant. Hence, appropriate policies for emission reduction could have a further beneficial effect on population health. Studies based on routine data and local effect estimates are recommended to properly inform the policy-making process.

We developed a novel indicator, daily excessive concentration hours (DECH), to explore the acute mortality impacts of ambient fine particulate matter pollution (PM2.5) in Hong Kong. The DECH of PM2.5 was calculated as daily concentration-hours >25 μg/m3. We applied a generalized additive models to quantify the association between DECH and mortality with adjustment for potential confounders. The results showed that the DECH was significantly associated with mortality. The excess mortality risk for an interquartile range (565 μg/m3*hours) increase in DECH of PM2.5 was 1.65% (95% CI: 1.05%, 2.26%) for all natural mortality at lag 02 day, 2.01% (95% CI: 0.82%, 3.21%) for cardiovascular mortality at lag 03 days, and 1.41% (95% CI: 0.34%, 2.49%) for respiratory mortality at lag 2 day. The associations remained consistent after adjustment for gaseous air pollutants (daily mean concentration of SO2, NO2 and O3) and in alternative model specifications. When compared to the mortality burden of daily mean PM2.5, DECH was found to be a relatively conservative indicator. This study adds to the evidence by showing that daily excessive concentration hours of PM2.5 might be a new predictor of mortality in Hong Kong.

In Yucatan, Mexico, chronic exposure of Mayan population to pesticides is expected as about 30 per cent are drinking polluted water. Residues of organochlorine pesticides (OCP) were monitored in 18 municipalities of Yucatan with high mortality rates due to uterine cervix cancer. 70 blood samples collected from Mayan women living in livestock, agricultural and metropolitan area were analyzed for OCP. Solid Phase Extraction was performed on C18 cartridges and analyzed by Gas Chromatography with Electron Capture Detector. The results showed that the highest OCP levels were detected in blood of women living in the livestock area. OCP detected were endosulfan I (7.35 μg/mL), aldrin (3.69 μg/mL), 4,4′ DDD (2.33 μg/mL), 1.39 and 1.46 μg/mL of δ-HCH. Women from the agricultural area had high concentrations of OCP in their blood, particularly dieldrin (1.19 μg/mL), and 1.26 μg/mL of 4,4′ DDE. In the metropolitan area, 0.080 μg/mL of γ-HCH and 0.064 μg/mL of heptachlore were detected. This monitoring study was also based on epidemiological data of uterine cervical cancer. It was found that environmental factors may have facilitated the infiltration of OCP to the aquifer used for potable water supply. These factors in addition to poverty can have impacts on public health. This first exploratory study suggests that monitoring of OCP in human is important for the establishment of health promotion programs. The integrative analysis of both, environmental and social factors would be helpful to characterize the bioaccumulation of pesticides in humans.

Vigorous air pollution control measures were implemented during the 2014 Asia-Pacific Economic Cooperation and a large-scale military parade (described here as “APEC Blue” and “Parade Blue” periods) in Beijing, China. A natural experiment was conducted in a health impact assessment framework to estimate the number of deaths attributable to PM2.5, using concentration-response functions derived from previous studies conducted in Beijing, combined with the differences in PM2.5 concentrations between intervention and reference periods. Substantial reductions in daily PM2.5 concentrations were observed during both intervention periods. Using the same dates from the prior year as a reference, daily PM2.5 concentration decreased from 98.57 μg/m³ to 47.53 μg/m³ during “APEC Blue”, and from 59.15 μg/m³ to 17.07 μg/m³ during the “Parade Blue”. We estimated that 39–63 all-cause deaths (21–51 cardiovascular, 6–13 respiratory deaths) have been prevented during the APEC period; and 41–65 deaths (22–52 cardiovascular, 6–13 respiratory deaths) have been prevented during the Parade period. This study shows that substantial mortality reductions could be achieved by implementing stringent air pollution mitigation measures.

There is limited evidence showing the mortality effects of temperature variability (TV) on cardiovascular diseases. The joint effects between TV and air pollutants are also less well-established. This study aims to assess the effect modification of TV-cardiovascular mortality by air pollutants in three Chinese cities (Beijing, Nanjing and Chengdu). Data of daily mortality, air pollutants and meteorological factors from 2008 to 2011 was collected from each city. TV was calculated as the standard deviation of daily maximum and minimum temperatures over exposure days. The city-specific effect estimates of TV on cardiovascular mortality were calculated using a quasi-Poisson regression model, adjusting for potential confounders (e.g., seasonality and temperature). An interaction term of TV and a three-level air pollutants stratum indicator was included in the models. Effect modifications by air pollutants were assessed by comparing the estimates of TV's effect between pollutant stratums and calculating the corresponding 95% confidential interval of the differences. Multivariate meta-analysis was conducted to obtain the pooled estimates. The data showed that TV was associated with increased risk of cardiovascular mortality, especially for longer TV exposure days (0–8 days, TV08). This association was still observed after adjusting for air pollutants on current day or the previous two days. Stronger estimates were observed in females, but no significant difference between males and females was detected, indicating the absence of evidence of effect modification by gender. Estimates of TV-cardiovascular mortality varied across two season periods (warm and cool season) and age groups, but the evidence of effect modification by age and seasons was absent. Regarding the effect modification of TV-cardiovascular mortality association by air pollutants, a significant effect modification was identified for PM10, but not for NO2 and SO2 in the whole population for all TV exposure days. This finding also persisted in subgroups, specifically in females and the elderly.