It is well established that anthropogenic chlorine-containing chemicals contribute to ozone layer depletion. The successful implementation of the Montreal Protocol has led to reductions in the atmospheric concentration of many ozone-depleting gases, such as chlorofluorocarbons. As a consequence, stratospheric chlorine levels are declining and ozone is projected to return to levels observed pre-1980 later this century. However, recent observations show the atmospheric concentration of dichloromethane-an ozone-depleting gas not controlled by the Montreal Protocol-is increasing rapidly. Using atmospheric model simulations, we show that although currently modest, the impact of dichloromethane on ozone has increased markedly in recent years and if these increases continue into the future, the return of Antarctic ozone to pre-1980 levels could be substantially delayed. Sustained growth in dichloromethane would therefore offset some of the gains achieved by the Montreal Protocol, further delaying recovery of Earth’s ozone layer.
Sea-level rise is a major consequence of climate change that will continue long after emissions of greenhouse gases have stopped. The 2015 Paris Agreement aims at reducing climate-related risks by reducing greenhouse gas emissions to net zero and limiting global-mean temperature increase. Here we quantify the effect of these constraints on global sea-level rise until 2300, including Antarctic ice-sheet instabilities. We estimate median sea-level rise between 0.7 and 1.2 m, if net-zero greenhouse gas emissions are sustained until 2300, varying with the pathway of emissions during this century. Temperature stabilization below 2 °C is insufficient to hold median sea-level rise until 2300 below 1.5 m. We find that each 5-year delay in near-term peaking of CO2emissions increases median year 2300 sea-level rise estimates by ca. 0.2 m, and extreme sea-level rise estimates at the 95th percentile by up to 1 m. Our results underline the importance of near-term mitigation action for limiting long-term sea-level rise risks.
The U.S. health care sector is highly interconnected with industrial activities that emit much of the nation’s pollution to air, water, and soils. We estimate emissions directly and indirectly attributable to the health care sector, and potential harmful effects on public health. Negative environmental and public health outcomes were estimated through economic input-output life cycle assessment (EIOLCA) modeling using National Health Expenditures (NHE) for the decade 2003-2013 and compared to national totals. In 2013, the health care sector was also responsible for significant fractions of national air pollution emissions and impacts, including acid rain (12%), greenhouse gas emissions (10%), smog formation (10%) criteria air pollutants (9%), stratospheric ozone depletion (1%), and carcinogenic and non-carcinogenic air toxics (1-2%). The largest contributors to impacts are discussed from both the supply side (EIOLCA economic sectors) and demand side (NHE categories), as are trends over the study period. Health damages from these pollutants are estimated at 470,000 DALYs lost from pollution-related disease, or 405,000 DALYs when adjusted for recent shifts in power generation sector emissions. These indirect health burdens are commensurate with the 44,000-98,000 people who die in hospitals each year in the U.S. as a result of preventable medical errors, but are currently not attributed to our health system. Concerted efforts to improve environmental performance of health care could reduce expenditures directly through waste reduction and energy savings, and indirectly through reducing pollution burden on public health, and ought to be included in efforts to improve health care quality and safety.
- Proceedings of the National Academy of Sciences of the United States of America
- Published about 8 years ago
We perform a multimodel detection and attribution study with climate model simulation output and satellite-based measurements of tropospheric and stratospheric temperature change. We use simulation output from 20 climate models participating in phase 5 of the Coupled Model Intercomparison Project. This multimodel archive provides estimates of the signal pattern in response to combined anthropogenic and natural external forcing (the fingerprint) and the noise of internally generated variability. Using these estimates, we calculate signal-to-noise (S/N) ratios to quantify the strength of the fingerprint in the observations relative to fingerprint strength in natural climate noise. For changes in lower stratospheric temperature between 1979 and 2011, S/N ratios vary from 26 to 36, depending on the choice of observational dataset. In the lower troposphere, the fingerprint strength in observations is smaller, but S/N ratios are still significant at the 1% level or better, and range from three to eight. We find no evidence that these ratios are spuriously inflated by model variability errors. After removing all global mean signals, model fingerprints remain identifiable in 70% of the tests involving tropospheric temperature changes. Despite such agreement in the large-scale features of model and observed geographical patterns of atmospheric temperature change, most models do not replicate the size of the observed changes. On average, the models analyzed underestimate the observed cooling of the lower stratosphere and overestimate the warming of the troposphere. Although the precise causes of such differences are unclear, model biases in lower stratospheric temperature trends are likely to be reduced by more realistic treatment of stratospheric ozone depletion and volcanic aerosol forcing.
Countries export much of the harm created by their greenhouse gas (GHG) emissions because the Earth’s atmosphere intermixes globally. Yet, the extent to which this leads to inequity between GHG emitters and those impacted by the resulting climate change depends on the distribution of climate vulnerability. Here, we determine empirically the relationship between countries' GHG emissions and their vulnerability to negative effects of climate change. In line with the results of other studies, we find an enormous global inequality where 20 of the 36 highest emitting countries are among the least vulnerable to negative impacts of future climate change. Conversely, 11 of the 17 countries with low or moderate GHG emissions, are acutely vulnerable to negative impacts of climate change. In 2010, only 28 (16%) countries had an equitable balance between emissions and vulnerability. Moreover, future emissions scenarios show that this inequality will significantly worsen by 2030. Many countries are manifestly free riders causing others to bear a climate change burden, which acts as a disincentive for them to mitigate their emissions. It is time that this persistent and worsening climate inequity is resolved, and for the largest emitting countries to act on their commitment of common but differentiated responsibilities.
Through this work, we have elucidated the mechanism of hydroxyl radicals (OH(•)) generation and its life time measurements in biosolution. We observed that plasma-initiated ultraviolet (UV) photolysis were responsible for the continues generation of OH(•) species, that resulted in OH(•) to be major reactive species (RS) in the solution. The density and lifetime of OH(•) species acted inversely proportional to each other with increasing depth inside the solution. The cause of increased lifetime of OH(•) inside the solution is predicted using theoretical and semiempirical calculations. Further, to predict the mechanism of conversion of hydroxide ion (OH(-)) to OH(•) or H2O2 (hydrogen peroxide) and electron, we determined the current inside the solution of different pH. Additionally, we have investigated the critical criterion for OH(•) interaction on cancer cell inducing apoptosis under effective OH(•) exposure time. These studies are innovative in the field of plasma chemistry and medicine.
Industrial chlorofluorocarbons that cause ozone depletion have been phased out under the Montreal Protocol. A chemically-driven increase in polar ozone (or “healing”) is expected in response to this historic agreement. Observations and model calculations taken together indicate that the onset of healing of Antarctic ozone loss has now emerged in September. Fingerprints of September healing since 2000 are identified through (i) increases in ozone column amounts, (ii) changes in the vertical profile of ozone concentration, and (iii) decreases in the areal extent of the ozone hole. Along with chemistry, dynamical and temperature changes contribute to the healing, but could represent feedbacks to chemistry. Volcanic eruptions episodically interfere with healing, particularly during 2015 (when a record October ozone hole occurred following the Calbuco eruption).
Association between Fine Particulate Air Pollution and Daily Clinic Visits for Migraine in a Subtropical City: Taipei, Taiwan
- International journal of environmental research and public health
- Published over 5 years ago
This study was undertaken to determine whether there was an association between fine particle (PM2.5) levels and daily clinic visits for migraine in Taipei, Taiwan. Daily clinic visits for migraine and ambient air pollution data for Taipei were obtained for the period from 2006-2011. The odds ratio of clinic visits was estimated using a case-crossover approach, controlling for weather variables, day of the week, seasonality, and long-term time trends. Generally, no significant associations between PM2.5 levels and migraine visits were observed on cool days. On warm days, however, for the single pollutant model (without adjustment for other pollutants), increased clinic visits for migraine were significantly associated with PM2.5 levels, with an interquartile range (IQR) rise associated with a 13% (95% CI = 8%-19%) elevation in number of migraine visits. In bi-pollutant model, PM2.5 remained significant after the inclusion of sulfur dioxide (SO2) or ozone (O3) on warm days. This study provides evidence that higher levels of PM2.5 increase the risk of clinic visits for migraine in Taipei, Taiwan.
A gap in emission inventories of urban volatile organic compound (VOC) sources, which contribute to regional ozone and aerosol burdens, has increased as transportation emissions in the United States and Europe have declined rapidly. A detailed mass balance demonstrates that the use of volatile chemical products (VCPs)-including pesticides, coatings, printing inks, adhesives, cleaning agents, and personal care products-now constitutes half of fossil fuel VOC emissions in industrialized cities. The high fraction of VCP emissions is consistent with observed urban outdoor and indoor air measurements. We show that human exposure to carbonaceous aerosols of fossil origin is transitioning away from transportation-related sources and toward VCPs. Existing U.S. regulations on VCPs emphasize mitigating ozone and air toxics, but they currently exempt many chemicals that lead to secondary organic aerosols.
Objective To investigate the relation between exposure to both air and noise pollution from road traffic and birth weight outcomes.Design Retrospective population based cohort study.Setting Greater London and surrounding counties up to the M25 motorway (2317 km2), UK, from 2006 to 2010.Participants 540 365 singleton term live births.Main outcome measures Term low birth weight (LBW), small for gestational age (SGA) at term, and term birth weight.Results Average air pollutant exposures across pregnancy were 41 μg/m3 nitrogen dioxide (NO2), 73 μg/m3 nitrogen oxides (NOx), 14 μg/m3 particulate matter with aerodynamic diameter <2.5 μm (PM2.5), 23 μg/m3 particulate matter with aerodynamic diameter <10 μm (PM10), and 32 μg/m3 ozone (O3). Average daytime (LAeq,16hr) and night-time (Lnight) road traffic A-weighted noise levels were 58 dB and 53 dB respectively. Interquartile range increases in NO2, NOx, PM2.5, PM10, and source specific PM2.5 from traffic exhaust (PM2.5 traffic exhaust) and traffic non-exhaust (brake or tyre wear and resuspension) (PM2.5 traffic non-exhaust) were associated with 2% to 6% increased odds of term LBW, and 1% to 3% increased odds of term SGA. Air pollutant associations were robust to adjustment for road traffic noise. Trends of decreasing birth weight across increasing road traffic noise categories were observed, but were strongly attenuated when adjusted for primary traffic related air pollutants. Only PM2.5 traffic exhaust and PM2.5 were consistently associated with increased risk of term LBW after adjustment for each of the other air pollutants. It was estimated that 3% of term LBW cases in London are directly attributable to residential exposure to PM2.5>13.8 μg/m3during pregnancy.Conclusions The findings suggest that air pollution from road traffic in London is adversely affecting fetal growth. The results suggest little evidence for an independent exposure-response effect of traffic related noise on birth weight outcomes.