Toxicity and human health assessment of an alcohol-to-jet (ATJ) synthetic kerosene developed under an international agreement with Sweden.

Alcohol-to-jet (ATJ) Synthetic Kerosene with Aromatics (SKA) fuels are produced by dehydration and refining of alcohol feed stocks. ATJ SKA fuel known as SB-8 was developed by Swedish Biofuels as a cooperative agreement between Sweden and AFRL/RQTF. SB-8 including standard additives was tested in a 90-day toxicity study with male and female Fischer 344 rats exposed to 0, 200, 700, or 2000 mg/m3 fuel in an aerosol/vapor mixture for 6 hr/day, 5 days/week. Aerosols represented 0.04 and 0.84% average fuel concentration in 700 or 2000 mg/m3 exposure groups. Examination of vaginal cytology and sperm parameters found no marked changes in reproductive health. Neurobehavioral effects were increased rearing activity (motor activity) and significantly decreased grooming (functional observational battery) in 2000 mg/m3 female rats. Hematological changes were limited to elevated platelet counts in 2000 mg/m3 exposed males. Minimal focal alveolar epithelial hyperplasia with increased number of alveolar macrophages was noted in some 2000 mg/m3 males and one female rat. Additional rats tested for genotoxicity by micronucleus (MN) formation did not detect bone marrow cell toxicity or alterations in number of MN; SB-8 was not clastogenic. Inhalation results were similar to effects reported for JP-8. Both JP-8 and SB fuels were moderately irritating under occlusive wrapped conditions but slightly irritating under semi-occlusion. Exposure to SB-8, alone or as 50:50 blend with petroleum-derived JP-8, is not likely to enhance adverse human health risks in the military workplace.

Combine effect of exposure to petrol, kerosene and diesel fumes: On hepatic oxidative stress and haematological function in rats.

Petroleum product fumes (PPFs) containing toxic organic components are pervasive in the environment, emanating from anthropogenic activities, including petroleum exploration and utilization by end-user activities from petrol-gasoline stations. Petrol station attendants are exposed to PPF through inhalation and dermal contact with consequent toxicological implications. We investigated the effects of chronic exposure (60 and 90 days) to petrol (P), kerosene (K) and diesel (D) alone and combined exposure to petrol, kerosene and diesel (PKD) fumes on hepatotoxicity, haematological function and oxidative stress in rats. Following sacrifice, we evaluated hepatic damage biomarkers, blood glucose, oxidative stress and haematological function. Chronic exposure to PPF significantly increased organo-somatic indices, blood glucose, biomarkers of hepatic toxicity and oxidative stress in an exposure duration-dependent manner. There was a simultaneous decrease in the protective capacity of antioxidants. Furthermore, exposure to PPF increased pro-inflammatory biomarkers in rats (90 > 60 days). Regardless of exposure duration, plateletcrit, mean platelet volume, platelet distribution width and red cell distribution width in the coefficient of variation increased, whereas red blood cell count, haemoglobin, packed cell volume, mean corpuscular volume, mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration, white blood cell, lymphocyte, monocyte-basophil-eosinophil mixed counts and platelet count decreased after 60 and 90 days exposure. Microscopic examination of the liver demonstrated hepatic pathological changes paralleling the duration of exposure to PKD fumes. However, the injury observed was lesser to that of rats treated with the diethylnitrosamine - positive control. Our results expanded previous findings and further demonstrated the probable adverse effect on populations' health occasioned by persistent exposure to PPF. Individuals chronically exposed by occupation to PPF may be at greater risk of developing disorders promoted by continuous oxido-inflammatory perturbation and suboptimal haematological-immunologic function - thereby enabling a permissive environment for pathogenesis notwithstanding the limitation of quantifying PPF absolute values in our model system.

Toxicity and human health assessment of an alcohol-to-jet (ATJ) synthetic kerosene.

A toxicological investigation was conducted for alcohol-to-jet (ATJ) fuels intended as a 50:50 blend with petroleum-derived fuel Jet Propulsion (JP)-8. The ATJ synthetic paraffinic kerosene (SPK) fuel was produced by Gevo (Englewood CO) and derived either from biomass (bio) or non-biomass sources. All toxicity tests were performed with one or both ATJ fuels following addition of a standard additive package required for JP-8. The primary fuel, Gevo (bio) ATJ SPK produced from biomass-derived iso-butanol, exhibited the same dermal irritation potential in rabbits as JP-8; the non-biomass-derived fuel was less irritating. The Gevo (bio) fuel was non-clastogenic in micronucleus testing with rats and neither version was mutagenic in the bacterial reverse mutation assay. A 90-day study was performed with Gevo (bio) ATJ SPK by exposing male and female Fischer 344 rats to target concentrations of 0, 200, 700 or 2000 mg/m3 of fuel, 6 hr per day, 5 days a week for 69 exposure days and included neurobehavioral assays and reproductive health evaluations in the study design. Results were negative or limited to irritant effects in the respiratory system due to exposure to a vapor and aerosol mixture in the 2000 mg/m3 exposure group. Occupational exposure limits for JP-8 were proposed for these ATJ fuels since these fuels display similar or somewhat lower toxicity than JP-8. As both versions of the Gevo ATJ jet fuel were similar, handling of either fuel alone or in a blend with petroleum-derived JP-8 appears unlikely to increase human health risks for workers.

Adverse health impacts of cooking with kerosene: A multi-country analysis within the Prospective Urban and Rural Epidemiology Study.

BACKGROUND: Kerosene, which was until recently considered a relatively clean household fuel, is still widely used in low- and middle-income countries for cooking and lighting. However, there is little data on its health effects. We examined cardiorespiratory effects and mortality in households using kerosene as their primary cooking fuel within the Prospective Urban Rural Epidemiology (PURE) study. METHODS: We analyzed baseline and follow-up data on 31,490 individuals from 154 communities in China, India, South Africa, and Tanzania where there was at least 10% kerosene use for cooking at baseline. Baseline comorbidities and health outcomes during follow-up (median 9.4 years) were compared between households with kerosene versus clean (gas or electricity) or solid fuel (biomass and coal) use for cooking. Multi-level marginal regression models adjusted for individual, household, and community level covariates. RESULTS: Higher rates of prevalent respiratory symptoms (e.g. 34% [95% CI:15-57%] more dyspnea with usual activity, 44% [95% CI: 21-72%] more chronic cough or sputum) and lower lung function (differences in FEV1: -46.3 ml (95% CI: -80.5; -12.1) and FVC: -54.7 ml (95% CI: -93.6; -15.8)) were observed at baseline for kerosene compared to clean fuel users. The odds of hypertension was slightly elevated but no associations were observed for blood pressure. Prospectively, kerosene was associated with elevated risks of all-cause (HR: 1.32 (95% CI: 1.14-1.53)) and cardiovascular (HR: 1.34 (95% CI: 1.00-1.80)) mortality, as well as major fatal and incident non-fatal cardiovascular (HR: 1.34 (95% CI: 1.08-1.66)) and respiratory (HR: 1.55 (95% CI: 0.98-2.43)) diseases, compared to clean fuel use. Further, compared to solid fuel users, those using kerosene had 20-47% higher risks for the above outcomes. CONCLUSIONS: Kerosene use for cooking was associated with higher rates of baseline respiratory morbidity and increased risk of mortality and cardiorespiratory outcomes during follow-up when compared to either clean or solid fuels. Replacing kerosene with cleaner-burning fuels for cooking is recommended.

Effect of household air pollution due to solid fuel combustion on childhood respiratory diseases in a semi urban population in Sri Lanka.

BACKGROUND: Household air pollution from combustion of solid fuels for cooking and space heating is one of the most important risk factors of the global burden of disease. This study was aimed to determine the association between household air pollution due to combustion of biomass fuel in Sri Lankan households and self-reported respiratory symptoms in children under 5 years. METHODS: A prospective study was conducted in the Ragama Medical Officer of Health area in Sri Lanka. Children under 5 years were followed up for 12 months. Data on respiratory symptoms were extracted from a symptom diary. Socioeconomic data and the main fuel type used for cooking were recorded. Air quality measurements were taken during the preparation of the lunch meal over a 2-h period in a subsample of households. RESULTS: Two hundred and sixty two children were followed up. The incidence of infection induced asthma (RR = 1.77, 95%CI;1.098-2.949) was significantly higher among children resident in households using biomass fuel and kerosene (considered as the high exposure group) as compared to children resident in households using Liquefied Petroleum Gas (LPG) or electricity for cooking (considered as the low exposure group), after adjusting for confounders. Maternal education was significantly associated with the incidence of infection induced asthma after controlling for other factors including exposure status. The incidence of asthma among male children was significantly higher than in female children (RR = 1.17; 95% CI 1.01-1.37). Having an industry causing air pollution near the home and cooking inside the living area were significant risk factors of rhinitis (RR = 1.39 and 2.67, respectively) while spending less time on cooking was a protective factor (RR = 0.81). Houses which used biomass fuel had significantly higher concentrations of carbon monoxide (CO) (mean 2.77 ppm vs 1.44 ppm) and particulate matter2.5 (PM2.5) (mean 1.09 mg/m3 vs 0.30 mg/m3) as compared to houses using LPG or electricity for cooking. CONCLUSION: The CO and PM2.5 concentrations were significantly higher in households using biomass fuel for cooking. There was a 1.6 times higher risk of infection induced asthma (IIA) among children of the high exposure group as compared to children of the low exposure group, after controlling for other factors. Maternal education was significantly associated with the incidence of IIA after controlling for exposure status and other variables.

Occupational exposure to petroleum-based and oxygenated solvents and oral and oropharyngeal cancer risk in men: A population-based case-control study in France.

OBJECTIVE: To examine the association between occupational exposure to petroleum-based and oxygenated solvents and the risk of oral and oropharyngeal cancer. METHODS: The ICARE study is a large population-based case-control study conducted in France between 2001 and 2007. This present analysis was restricted to men and included 350 and 543 cases of squamous cell-carcinoma of the oral cavity and oropharynx, respectively, and 2780 controls. Lifetime tobacco, alcohol consumption and complete occupational history were assessed through detailed questionnaires. Job-exposure matrices allowed us to assess occupational exposure to five petroleum-based solvents (white spirits; diesel/fuel oils/kerosene; gasoline; benzene; special petroleum products) and five oxygenated solvents (diethyl ether; tetrahydrofuran; ketones and esters; alcohols; ethylene glycol). Odds-ratios (ORs), adjusted for age, smoking, alcohol consumption and socioeconomic status, and 95% confidence intervals (CI) were estimated using unconditional logistic models. RESULTS: Associations between oral cancer risk and exposure to white spirits and diesel/fuel oils/kerosene were suggested, but there was no exposure-response trend. Concerning exposure to oxygenated solvents, participants with the highest levels of cumulative exposure to diethyl ether had a significant excess risk of oropharyngeal cancer (OR = 7.78, 95%CI 1.42 to 42.59; p for trend = 0.04). Ever exposure to tetrahydrofuran was associated with a borderline significant increased risk of oral cancer (OR = 1.87, 95%CI 0.97 to 3.61), but no exposure-response trend was observed. Additional adjustments for exposure to other solvents did not substantially change the results. CONCLUSION: Our results do not provide evidence for a major role of petroleum-based and oxygenated solvents in the occurrence of oral and oropharyngeal cancers in men.

Executive summary workshop: toward the elimination of the use of solid fuels and kerosene in urban homes in the americas

Household air pollution is one of the principal causes of disease and premature death in low and middle-income countries (LMIC) and is an avoidable health risk. In the Americas, the World Health Organization (WHO) estimated that approximately 82,000 deaths in these countries were attributale to cooking, heating, and lighting with polluting fuels and technologies in 2016. Accelerating the transition to clean energy for all is an urgent and necessary public health intervention in the region of the Americas, to reduce the health risks that primarily affect socially and economically vulnerable populations, to achieve a continent healthier, more equitable and with sustainable development, contributing to the worldwide efforts to achieve the Sustainable Development Goals (SDGs) by 2030. To achieve this result, the health sector should be involved in the design of policy interventions to reduce exposure to indoor air pollution and its effects on health, as well associal inequities. In line with the WHO Indoor Air Quality Guidelines launched in November 2014, the PAHO Strategic Plan 2014-2019 has set itself the objective of helping Member States to reduce the percentage of population by 5% that depends on solid fuels for cooking in countries with a percentage of users equal to or greater than 10% of the population (priority countries). To measure progress, one indicator is the number of countries that are implementing large-scale programs to reduce solid fuel use (SFU) in the home, and a outcome indicator measures progress in the use of energy and clean technology for cooking at home. Evaluating the progress of the countries in the indicator of the Strategic Plan, some of its member states have successfully reduced solid fuel use (SFU) in the households by 5% and have implemented large-scale programs to transition to clean fuels. Nevertheless, in other countries in the region, progress has been almost non-existent. Following the first workshop carried out in Tegucigalpa (Honduras) in 2015, where new indoor air pollution guidelines were launched by the WHO, the workshop "Toward the elimination of solid fuels and kerosene in urban homes in the Americas" was organized and carried out in Mexico City (Mexico) from September 11 to 13, 2018.

Toxicity and occupational exposure assessment for Fischer-Tropsch synthetic paraffinic kerosene.

Fischer-Tropsch (FT) Synthetic Paraffinic Kerosene (SPK) jet fuel is a synthetic organic mixture intended to augment petroleum-derived JP-8 jet fuel use by the U.S. armed forces. The FT SPK testing program goal was to develop a comparative toxicity database with petroleum-derived jet fuels that may be used to calculate an occupational exposure limit (OEL). Toxicity investigations included the dermal irritation test (FT vs. JP-8 vs. 50:50 blend), 2 in vitro genotoxicity tests, acute inhalation study, short-term (2-week) inhalation range finder study with measurement of bone marrow micronuclei, 90-day inhalation toxicity, and sensory irritation assay. Dermal irritation was slight to moderate. All genotoxicity studies were negative. An acute inhalation study with F344 rats exposed at 2000 mg/m3 for 4 hr resulted in no abnormal clinical observations. Based on a 2-week range-finder, F344 rats were exposed for 6 hr per day, 5 days per week, for 90 days to an aerosol-vapor mixture of FT SPK jet fuel (0, 200, 700 or 2000 mg/m3). Effects on the nasal cavities were minimal (700 mg/m3) to mild (2000 mg/m3); only high exposure produced multifocal inflammatory cell infiltration in rat lungs (both genders). The RD50 (50% respiratory rate depression) value for the sensory irritation assay, calculated to be 10,939 mg/m3, indicated the FT SPK fuel is less irritating than JP-8. Based upon the proposed use as a 50:50 blend with JP-8, a FT SPK jet fuel OEL is recommended at 200 mg/m3 vapor and 5 mg/m3 aerosol, in concurrence with the current JP-8 OEL.

Assessment of DNA damage in blood lymphocytes of bakery workers by comet assay.

The comet assay is widely used in screening and identification of genotoxic effects of different substances on people in either their working or living environment. Exposure to fuel smoke leads to DNA damage and ultimately different types of cancer. Using a comet assay, the present study aimed to assess peripheral blood lymphocyte DNA damage in people working in bakeries using natural gas, kerosene, diesel, or firewood for fuel compared to those in the control group. The subjects of this study were 55 people in total who were divided into four experimental groups, each of which comprised of 11 members (based on the type of fuel used), and one control group comprised of 11 members. Using CometScore, the subjects' peripheral blood lymphocytes were examined for DNA damage. All bakers, that is, experimental subjects, showed significantly greater peripheral blood lymphocyte DNA damage compared to the individuals in the control group. There was greater peripheral blood lymphocyte DNA damage in bakers who had been using firewood for fuel compared to those using other types of fuel to such an extent that tail moments (µm) for firewood-burning bakers was 4.40 ± 1.98 versus 1.35 ± 0.84 for natural gas, 1.85 ± 1.33 for diesel, and 2.19 ± 2.20 for kerosene. The results indicated that burning firewood is the greatest inducer of peripheral blood lymphocytes DNA damage in bakers. Nonetheless, there was no significant difference in peripheral blood lymphocyte DNA damage among diesel and kerosene burning bakers.

Lung injury via oxidative stress in mice induced by inhalation exposure to rocket kerosene.

Rocket kerosene (RK) is a new rocket propellant. Toxicity occurs if a high level of RK is inhaled. To study the toxicity of RK in lung and the mechanisms of RK-induced lung jury, a total of 72 male ICR mice (1.5 months, adult) were randomly assigned to the RK exposure group (RKEG) and normal control group (NCG). Mice were whole-body exposed to room air or aerosol of 18000 mg/m3 RK for 4 hours. Histopathological analysis was performed to evaluate the pulmonary lesions. Oxidative stress was assessed by assay of MDA, SOD, GSH-PX and TAOC. Inflammatory response was estimated by detecting inflammatory cell counts, TNF-α and IL-6 protein levels in serum. The results showed that after 2 to 6 hours of RK exposure, pulmonary vascular dilatation, congestion and edematous widening of the alveolar septum were noted. After 12 to 24 hours post-exposure, diffuse hemorrhage in alveolar space were found, along with the progressive pulmonary vascular dilatation and edematous widening of alveolar septum. During 3 to 7 days of RK-exposure, inflammatory cells were scattered in the lung tissue. The pathological alterations of the lung were alleviated after 14 days post-exposure, and showed significant improvement after 21 days post-exposure. After 30 days of RK exposure, the pathological changes in the lung tissue were nearly recovered except the local thickening of the alveolar wall. Compared with NCG, RK inhalation produced a significant increase of MDA levels and a significant decrease of SOD, GSH-Px and TAOC activity in the lung after 2 hours post-exposure (P<0.05). There were significant increases of TNF-α and IL-6 protein levels in serum of mice in RKEG after 2, 6 and 12 hours and 1, 4 and 7 days post-exposure compared with NCG (P<0.05). TNF-α protein levels had a sharp increase after 4 days of exposure. IL-6 protein level was increased at early phase of experiment and then gradually decreased along with the prolonged course of exposure. Considering that the RK-induced lung injury was through the oxidative stress, inhibition of oxidative stress after RK exposure may be urgently needed.

Effects and mechanisms of kerosene use-related toxicity.

Kerosene is a heterogeneous hydrocarbon substance that continues to find many uses worldwide due to its economic viability and ease of availability. In spite of kerosene's many uses, it is known to cause harm to various body organs and systems. Major affected body organs/systems are the pulmonary system, central nervous system, cardiovascular system, the skin, immune system and liver. This review discusses the various kerosene-mediated adverse health effects and possible mechanisms by which kerosene is likely to inflict such effects. These mechanisms are quite varied and include induction of inflammation, loss of effectiveness of pulmonary surfactants, hypoxia, production of highly reactive oxidative metabolites, extraction of endogenous epidermal and membrane lipids, necrosis, hormonal and enzymatic levels changes, and immunosuppression. Understanding of the above will allow for proper relevant policy formulation and targeted kerosene-mediated morbidity and mortality preventive and management initiatives.

[Effects on blood cell numbers and cytokines of dermal application rocket kerosene in mice].

OBJECTIVE: To detect the number of cells and the level of IL-2, IL-4, IL-6, IL-10, TNF-alpha, IFN-γ and IL-17 cytokines in the peripheral blood of mice exposed to rocket kerosene by skin. METHOD: ICR mice were randomly divided into the normal control group and RK experimental group (400 µl×1 group). RK undiluted fuel were applied directly to the dorsal skin of the mice. In control groups were treated with sesame oil (SO). the number of blood cells were detected by automatic blood cell counter and the level of IL-2, IL-4, IL-6, IL-10, TNF-alpha, IFN-γ and IL-17 cytokines in serum were detected by using flow cytometry and BD CBA Flex set kit. RESULT: Compared with the normal group, WBC and LYM had a decreasing tendency 2 h and decreased significantly 6 h, 12 h and 1 d after RK exposure (P<0.05). They increased significantly 7 d after RK exposure (P<0.05). Compared with the normal group, the level of IL-6 increased significantly 2 h, 6 h, 12 h,1 d and 3 d (P<0.05). The level of TNF-α increased significantly 2h, 3d, 5d and 7d (P<0.05). The level of IL-10 increased significantly 2 h, 6 h, 3 d, 5 d and 7 d (P<0.05). The level of IFN-γ increased significantly 6 h and 3 d (P< 0.05). The level of IL-17 significantly increased 3 d, 5 d and 7d (P<0.05). CONCLUSION: RK can change the number of immune cells, causing the immune cytokine changes in mice after RK cutaneous exposure.

Effects of diesel and kerosene on germination and growth of coastal wetland plant species.

This study aims to investigate effects of diesel and kerosene on seed germination and seedling growth among coastal wetland plants to select species that can be used for the restoration and revegetation of oil-polluted habitats. Tests on 51 species were performed in Petri dishes containing 0 %, 6 %, 12 %, and 18 % diesel, 20 %, 40 %, and 60 % kerosene; each treatment combination was replicated five times with 20 seeds in each Petri dish. All dishes were held in a growth chamber with 20°C day of 12 h/15°C night of 12 h in 80 % humidity for 20 days for calculating the germination percentage, seedling weight, and seedling vitality. The germination percentage of Rumex stenophyllus decreased significantly in diesel and kerosene treatments. The weights of seedlings treated with diesel and kerosene either increased or decreased in comparison with controls depending on the species. Vitality percentage values were high for seedlings of Chenopodium ficifolium. Thus, herbaceous plant responses to oil treatments are species-specific.

A 13-week dermal repeat-dose neurotoxicity study of hydrodesulfurized kerosene in rats.

A 13-week dermal repeat-dose toxicity study was conducted with hydrodesulfurized (HDS) kerosene, a test material that also met the commercial specifications for aviation turbine fuel (jet A). The objectives were to assess the potential for target organ toxicity and neurotoxicity. The HDS kerosene was applied to the shaved backs of Sprague-Dawley CD rats, 12/sex/group, 6 h/d, 5 d/wk in doses of 0 (vehicle control), 165 mg/kg (20% HDS kerosene), 330 mg/kg (40% HDS kerosene), or 495 mg/kg (60% HDS kerosene). Additional rats (12/sex) from the control and the high-dose groups were held without treatment for 4 weeks to assess recovery. Standard parameters of toxicity were investigated during the in-life phase. At necropsy, organs were weighed and selected tissues were processed for microscopic evaluation. Neurobehavioral evaluations included tests of motor activity and functional observations that were conducted pretest, at intervals during the exposure period and after recovery. No test substance-related effects on mortality, clinical observations (except dermal irritation), body weight, or clinical chemistry values were observed. A dose-related increase in skin irritation, confirmed histologically as minimal, was evident at the dosing site. The only statistically significant change considered potentially treatment related was an increase in the neutrophil count in females at 13 weeks. No test article-related effects were observed in the neurobehavioral assessments or gross or microscopic findings in the peripheral or central nervous system tissues in any of the dose groups. Excluding skin irritation, the no observed adverse effect level value for all effects was considered 495 mg/kg/d.

Jet fuel kerosene is not immunosuppressive in mice or rats following inhalation for 28 days.

Previous reports indicated that inhalation of JP-8 aviation turbine fuel is immunosuppressive. However, in some of those studies, the exposure concentrations were underestimated, and percent of test article as vapor or aerosol was not determined. Furthermore, it is unknown whether the observed effects are attributable to the base hydrocarbon fuel (jet fuel kerosene) or to the various fuel additives in jet fuels. The present studies were conducted, in compliance with Good Laboratory Practice (GLP) regulations, to evaluate the effects of jet fuel kerosene on the immune system, in conjunction with an accurate, quantitative characterization of the aerosol and vapor exposure concentrations. Two female rodent species (B6C3F1 mice and Crl:CD rats) were exposed by nose-only inhalation to jet fuel kerosene at targeted concentrations of 0, 500, 1000, or 2000 mg/m(3) for 6 h daily for 28 d. Humoral, cell-mediated, and innate immune functions were subsequently evaluated. No marked effects were observed in either species on body weights, spleen or thymus weights, the T-dependent antibody-forming cell response (plaque assay), or the delayed-type hypersensitivity (DTH) response. With a few exceptions, spleen cell numbers and phenotypes were also unaffected. Natural killer (NK) cell activity in mice was unaffected, while the NK assessment in rats was not usable due to an unusually low response in all groups. These studies demonstrate that inhalation of jet fuel kerosene for 28 d at levels up to 2000 mg/m(3) did not adversely affect the functional immune responses of female mice and rats.

Pyopneumothorax following suicidal kerosene ingestion.

Liquid hydrocarbons derived from petroleum are widely used in household and industry. Many hydrocarbons in kerosene, such as hexane, naphthalene, octane and phenanthrene, are toxic to humans. Pulmonary toxicity is the major cause of morbidity and mortality followed by central nervous-system and cardiovascular complications. As kerosene is a mixture of chemicals, there is no definitive absorption, distribution, metabolism and excretion. The major route of exposure is by inhalation of liquid (aspiration). Kerosene vapours may be mildly irritating to the respiratory system and spray applications of kerosene may provoke signs of pulmonary irritation such as coughing and dyspnoea. Kerosene aspiration leads to inflammation and loss of surfactant. Secondary effects in the lungs include pneumothorax, pneumatocele or bronchopleural fistula. Here, we are presenting a case of pyopneumothorax after kerosene consumption.

Kerosene: a review of household uses and their hazards in low- and middle-income countries.

Kerosene has been an important household fuel since the mid-19th century. In developed countries its use has greatly declined because of electrification. However, in developing countries, kerosene use for cooking and lighting remains widespread. This review focuses on household kerosene uses, mainly in developing countries, their associated emissions, and their hazards. Kerosene is often advocated as a cleaner alternative to solid fuels, biomass and coal, for cooking, and kerosene lamps are frequently used when electricity is unavailable. Globally, an estimated 500 million households still use fuels, particularly kerosene, for lighting. However, there are few studies, study designs and quality are varied, and results are inconsistent. Well-documented kerosene hazards are poisonings, fires, and explosions. Less investigated are exposures to and risks from kerosene's combustion products. Some kerosene-using devices emit substantial amounts of fine particulates, carbon monoxide (CO), nitric oxides (NO(x)), and sulfur dioxide (SO(2)). Studies of kerosene used for cooking or lighting provide some evidence that emissions may impair lung function and increase infectious illness (including tuberculosis), asthma, and cancer risks. However, there are few study designs, quality is varied, and results are inconsistent. Considering the widespread use in the developing world of kerosene, the scarcity of adequate epidemiologic investigations, the potential for harm, and the implications for national energy policies, researchers are strongly encouraged to consider collecting data on household kerosene uses in studies of health in developing countries. Given the potential risks of kerosene, policymakers may consider alternatives to kerosene subsidies, such as shifting support to cleaner technologies for lighting and cooking.

Single-nucleotide polymorphisms associated with skin naphthyl-keratin adduct levels in workers exposed to naphthalene.

BACKGROUND: Individual genetic variation that results in differences in systemic response to xenobiotic exposure is not accounted for as a predictor of outcome in current exposure assessment models. OBJECTIVE: We developed a strategy to investigate individual differences in single-nucleotide polymorphisms (SNPs) as genetic markers associated with naphthyl-keratin adduct (NKA) levels measured in the skin of workers exposed to naphthalene. METHODS: The SNP-association analysis was conducted in PLINK using candidate-gene analysis and genome-wide analysis. We identified significant SNP-NKA associations and investigated the potential impact of these SNPs along with personal and workplace factors on NKA levels using a multiple linear regression model and the Pratt index. RESULTS: In candidate-gene analysis, a SNP (rs4852279) located near the CYP26B1 gene contributed to the 2-naphthyl-keratin adduct (2NKA) level. In the multiple linear regression model, the SNP rs4852279, dermal exposure, exposure time, task replacing foam, age, and ethnicity all were significant predictors of 2NKA level. In genome-wide analysis, no single SNP reached genome-wide significance for NKA levels (all p ≥ 1.05 × 10(-5)). Pathway and network analyses of SNPs associated with NKA levels were predicted to be involved in the regulation of cellular processes and homeostasis. CONCLUSIONS: These results provide evidence that a quantitative biomarker can be used as an intermediate phenotype when investigating the association between genetic markers and exposure-dose relationship in a small, well-characterized exposed worker population.

Acute treatment with kerosene damages the dermal barrier and alters the distribution of topically applied benzo(a)pyrene in mice.

The dermal route is important in many occupational exposures. Some materials may reduce the barrier function of the skin to enhance absorption and effect on internal organs. We have reported previously that kerosene cleaning following treatment with used engine oil increased DNA adduct levels in the lungs of mice compared with animals treated with used oil alone. To investigate what other physiological parameters might be affected by kerosene, we conducted in vitro and in vivo measurements of skin barrier function. We also topically applied (3)H-BAP(100 nM in 25 µL acetone) and washed half the mice with 25 µL kerosene 1 hr after carcinogen application. Groups of four mice were euthanized from 1 to 72 hr after treatment. Skin, lungs, and livers were harvested from each animal and stored separately. Kerosene application reduced the barrier function of the skin in vitro beyond the effect of the acetone vehicle and the vehicle plus BAP. In vivo studies indicated that kerosene treatment reduced the barrier function at 4 and 8 hr post application and that the barrier function recovered at 24 hr after a single treatment. The fraction of the radiolabel remaining in the skin of animals treated with (3)H-BAP and washed with kerosene was significantly less than those not washed, beginning at 24 hr (p< 0.05). Fractional distribution to the lungs and livers of these animals became significantly elevated at this time. Kerosene treatment compromises dermal barrier function and the ability of the skin to retain water, enhances carcinogen absorption, and alters organ distribution. This appears to contribute to the increase in BAP DNA adducts we reported earlier.