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Laboratory exposures of persons with asthma to diesel exhaust are associated with physiological and clinical changes that are consistent with diminished disease control. In this trial, which involved persons with mild or moderate asthma, exposure to diesel exhaust during a walk on a London street was associated with physiological changes in lung function as compared with a walk in a nearby park. Exposure to diesel exhaust can result in worsening of asthma. In persons with mild or moderate asthma, exposure to diesel exhaust during a walk on a London street was associated with physiological changes in lung function as compared with a walk in a nearby park. Air pollution from road traffic is a serious health hazard, and particulates from diesel exhaust have become cause for increasing concern. Epidemiologic studies have demonstrated associations between ambient particulate matter and respiratory-associated morbidity and mortality; these effects may be greater among persons with preexisting respiratory disease, including asthma. 1 , 2 Diesel engines emit relatively low concentrations of carbon monoxide and carbon dioxide, but as compared with gasoline engines of similar size, diesel engines can generate more than 100 times the number of particles per distance traveled 3 and are major contributors to atmospheric particulate pollution. In urban environments, almost 90% of traffic-generated . . .

Vehicle emissions contribute to fine particulate matter (PM ) and tropospheric ozone air pollution, affecting human health, crop yields and climate worldwide. On-road diesel vehicles produce approximately 20 per cent of global anthropogenic emissions of nitrogen oxides (NO ), which are key PM and ozone precursors. Regulated NO emission limits in leading markets have been progressively tightened, but current diesel vehicles emit far more NO under real-world operating conditions than during laboratory certification testing. Here we show that across 11 markets, representing approximately 80 per cent of global diesel vehicle sales, nearly one-third of on-road heavy-duty diesel vehicle emissions and over half of on-road light-duty diesel vehicle emissions are in excess of certification limits. These excess emissions (totalling 4.6 million tons) are associated with about 38,000 PM - and ozone-related premature deaths globally in 2015, including about 10 per cent of all ozone-related premature deaths in the 28 European Union member states. Heavy-duty vehicles are the dominant contributor to excess diesel NO emissions and associated health impacts in almost all regions. Adopting and enforcing next-generation standards (more stringent than Euro 6/VI) could nearly eliminate real-world diesel-related NO emissions in these markets, avoiding approximately 174,000 global PM - and ozone-related premature deaths in 2040. Most of these benefits can be achieved by implementing Euro VI standards where they have not yet been adopted for heavy-duty vehicles.

Exposure to ambient fine particulate matter (PM 2.5 ) is a leading contributor to diseases in India. Previous studies analysing emission source attributions were restricted by coarse model resolution and limited PM 2.5 observations. We use a regional model informed by new observations to make the first high-resolution study of the sector-specific disease burden from ambient PM 2.5 exposure in India. Observed annual mean PM 2.5 concentrations exceed 100 μg m −3 and are well simulated by the model. We calculate that the emissions from residential energy use dominate (52%) population-weighted annual mean PM 2.5 concentrations, and are attributed to 511,000 (95UI: 340,000–697,000) premature mortalities annually. However, removing residential energy use emissions would avert only 256,000 (95UI: 162,000–340,000), due to the non-linear exposure–response relationship causing health effects to saturate at high PM 2.5 concentrations. Consequently, large reductions in emissions will be required to reduce the health burden from ambient PM 2.5 exposure in India. Exposure to ambient particulate matter is a key contributor to disease in India and source attribution is vital for pollution control. Here the authors use a high-resolution regional model to show residential emissions dominate particulate matter concentrations and associated premature mortality.

Environmental impacts of energy use can impose large costs on society. We quantify and monetize the life-cycle climate-change and health effects of greenhouse gas (GHG) and fine particulate matter (PM₂.₅) emissions from gasoline, corn ethanol, and cellulosic ethanol. For each billion ethanol-equivalent gallons of fuel produced and combusted in the US, the combined climate-change and health costs are $469 million for gasoline, $472-952 million for corn ethanol depending on biorefinery heat source (natural gas, corn stover, or coal) and technology, but only $123-208 million for cellulosic ethanol depending on feedstock (prairie biomass, Miscanthus, corn stover, or switchgrass). Moreover, a geographically explicit life-cycle analysis that tracks PM₂.₅ emissions and exposure relative to U.S. population shows regional shifts in health costs dependent on fuel production systems. Because cellulosic ethanol can offer health benefits from PM₂.₅ reduction that are of comparable importance to its climate-change benefits from GHG reduction, a shift from gasoline to cellulosic ethanol has greater advantages than previously recognized. These advantages are critically dependent on the source of land used to produce biomass for biofuels, on the magnitude of any indirect land use that may result, and on other as yet unmeasured environmental impacts of biofuels.

Background Anemia is a major global burden, and occupational gasoline exposure is a common occupational hazard factor. Although previous studies have shown that there is a potential relationship between occupational gasoline exposure and the increase of anemia prevalence, this relationship has not been fully explored. The current cohort study aimed to investigate the association between occupational exposure to gasoline and anemia, and the effect of gasoline concentration on hemoglobin (Hb) levels. Methods This retrospective cohort study collected baseline data from 1451 workers, including 605 exposed to gasoline and 846 not exposed to gasoline. Participants were enrolled in 2013–2015, and follow-up in 2019. Anemia was diagnosed according to WHO guidelines on hemoglobin cutoffs to define anemia in individuals and populations. Occupational exposure concentration of gasoline was measured based on the Chinese national standard (GBZ-T300.62-2017). Logistic regression was conducted to analyze the associations of occupational exposure to gasoline and anemia. Results The incidence of anemia among workers exposed to gasoline was significantly higher than that among non-exposed workers (relative risk [RR] = 11.03, 95% confidence interval [CI]: 9.45–12.53). The risks of anemia were significantly higher among participants exposed to gasoline concentrations ≥ 43.20 mg/m³ (RR = 13.92, 95%CI: 12.25–15.28), 18.01–43.19 mg/m³ (RR = 12.93, 95%CI: 11.07–14.51), and 0.01–18.00 mg/m³ (RR = 5.49, 95%CI: 3.96–7.32) compared with the control non-exposed group. The risk of anemia was significantly higher among exposed workers, after adjusting for all confounding factors. There was also a significant negative correlation between gasoline exposure concentration and hemoglobin level. Conclusions Occupational exposure to gasoline is associated with an increased incidence of anemia, with a positive correlation between occupational gasoline exposure levels and the severity of anemia. The incidence and severity of anemia increase while hemoglobin levels decrease in line with increasing gasoline exposure concentrations. These findings emphasize the importance of assessing anemia in workers exposed to gasoline.

The impact of health and environmental hazards, associated with the constituents of gasoline, on occupationally exposed workers has been recorded over the past few decades. However, the scientific literature on their pathogenic potential remains incomplete, which could affect the current understanding of the associated health risks. This review provides current information based on recently improved research techniques to evaluate gasoline toxicity profiles for humans. Our current knowledge provides insight into the intricate mechanism of gasoline-induced adverse effects, including the formation of reactive metabolites via bio-activation and subsequent generation of reactive oxygen species (ROS) and oxidative stress, which are involved in multiple mechanisms that are central to the aetiology of gasoline-induced toxicity. These mechanisms include covalent binding to deoxyribonucleic acid (DNA), leading to oxidative damage, tumor-suppression gene activity, and activation of pro-oncogenes. Furthermore, it results in induction of autoimmunity and local inflammatory responses, disruption of multiple neurotransmitters and immune cell function, derangement of various enzyme activities (e.g., sodiumpotassium adenosine triphosphate (Na+/K+/ATPase) activity, cytochrome P450 (CYP450), nitric oxide synthase (NOS), antioxidant enzyme activities, etc.), conjugation of bile, and non-specific cell membrane interaction, leading to damage of the membrane lipid bilayer and proteins. Available data suggests that exposure to gasoline or gasoline constituents have the potential to cause different types of illnesses. The data highlights the need to maintain safety measures via suitable research, medical surveillance, regulatory control, life style modification, early detection, and intervention to minimize exposure and manage suspected cases. They also present novel opportunities to design and develop effective therapeutic strategies against gasoline-induced detrimental effects. Int J Occup Med Environ Health 2017;30(1):1-26.

This study determined the susceptibility of cultured soil microorganisms to the effects of Ekodiesel Ultra fuel (DO), to the enzymatic activity of soil and to soil contamination with PAHs. Studies into the effects of any type of oil products on reactions taking place in soil are necessary as particular fuels not only differ in the chemical composition of oil products but also in the composition of various fuel improvers and antimicrobial fuel additives. The subjects of the study included loamy sand and sandy loam which, in their natural state, have been classified into the soil subtype 3.1.1 Endocalcaric Cambisols. The soil was contaminated with the DO in amounts of 0, 5 and 10 cm 3  kg −1 . Differences were noted in the resistance of particular groups or genera of microorganisms to DO contamination in loamy sand (LS) and sandy loam (SL). In loamy sand and sandy loam, the most resistant microorganisms were oligotrophic spore-forming bacteria. The resistance of microorganisms to DO contamination was greater in LS than in SL. It decreased with the duration of exposure of microorganisms to the effects of DO. The factor of impact (IF DO ) on the activity of particular enzymes varied. For dehydrogenases, urease, arylsulphatase and β-glucosidase, it had negative values, while for catalase, it had positive values and was close to 0 for acid phosphatase and alkaline phosphatase. However, in both soils, the noted index of biochemical activity of soil (BA) decreased with the increase in DO contamination. In addition, a positive correlation occurred between the degree of soil contamination and its PAH content.

Impacts of inhaling gasoline fumes on the lungs of adult male rats and the alleviating role of fenugreek seeds were evaluated. Twenty-four rats were divided into four groups, unexposed control and fenugreek groups, gasoline exposed groups for 6 h/6 day/week for 10 weeks with and without supplementation of fenugreek seed powder in food (5% w/w). Rats exposed to gasoline fumes showed significant elevation in lung tumor necrosis factor-α, as an inflammatory marker, and the proapoptotic marker Bax with a reduction in the antiapoptotic marker Bcl2. Moreover, remarkable elevations in transforming growth factor-β1, collagen and hydroxyproline were observed as fibrotic markers. Lung oxidative stress markers (hydrogen peroxides, malondialdehyde, and protein carbonyl) increased significantly along with marked decrease in total antioxidant capacity, superoxide dismutase, and catalase levels. Additionally, marked decreases in white and red blood cell counts, hemoglobin content, platelet count, accompanied by elevated red cell distribution width percentage were observed, supporting the inflammatory status. Histopathological changes represented by hematoxylin&eosin, immunohistochemistry staining for Bax&Bcl2, and transmission electron microscopy supported the negative impacts of gasoline fumes compared to the control group. Fenugreek seeds supplementation with gasoline exposure showed pronounced alleviation of lung biochemical and histopathological changes compared to the gasoline-exposed group.

Esophageal stricture is a narrowing of the esophageal lumen which is often characterized by impaired swallowing or dysphagia. It can be induced by inflammation, fibrosis or neoplasia which damages the mucosa and/or submucosa of the esophagus. Corrosive substance ingestion is one of the major causes of esophageal stricture, particularly in children and young adults. For instance, accidental ingestion or attempted suicide with corrosive household products is not uncommon. Gasoline is a liquid mixture of aliphatic hydrocarbons derived from the fractional distillation of petroleum, which is then combined with additives such as isooctane and aromatic hydrocarbons (e.g., toluene and benzene). Gasoline also contains several other additives including ethanol, methanol and formaldehyde, which make it a corrosive agent. Interestingly, to the best of our knowledge, the incidence of esophageal stricture caused by chronic gasoline ingestion has not been reported. In this paper, we report the case of a patient with dysphagia due to complex esophageal stricture due to chronic gasoline ingestion who underwent a series of esophago-gastro-duodenoscopy (EGD) procedures and repeated esophageal dilation.

We examined ambient exposure to specific air toxics in the perinatal period in relation to retinoblastoma development. Cases were ascertained from California Cancer Registry records of children diagnosed between 1990 and 2007 and matched to California birth certificates. Controls were randomly selected from state birth records for the same time period. We chose 27 air toxics for the present study that had been listed as possible, probable, or established human carcinogens by the International Agency for Research on Cancer. Children (103 cases and 30,601 controls) included in the study lived within 5 miles of an air pollution monitor. Using logistic regression analyses, we modeled the risk of retinoblastoma due to air toxic exposure, separately for exposures in pregnancy and the first year of life. With a per interquartile range increase in air toxic exposure, retinoblastoma risk was found to be increased with pregnancy exposure to benzene (OR=1.67, 95% CI: 1.06, 2.64) and other toxics which primarily arise from gasoline and diesel combustion: toluene, 1,3-butadiene, ethyl benzene, ortho-xylene, and meta/para-xylene; these six toxics were highly correlated. Retinoblastoma risk was also increased with pregnancy exposure to chloroform (OR=1.35, 95% CI: 1.07, 1.70), chromium (OR=1.29, 95% CI: 1.04, 1.60), para-dichlorobenzene (OR=1.24, 95% CI: 1.04, 1.49), nickel (OR=1.48, 95% CI: 1.08, 2.01), and in the first year of life, acetaldehyde (OR=1.62, 95% CI: 1.06, 2.48). Sources of these agents are discussed.