Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects

Lewtas, Joellen

doi:10.1016/j.mrrev.2007.08.003

Cited by 585 publications

(372 citation statements)

References 327 publications

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“…Moreover, also from the recent literature, PAHs are still considered the primary human cancer causative agents present in coal combustion emissions [for a comprehensive review see Ref. 36 and references therein]. On the other hand, it is known that some metals, in addition to genetic damage via both oxidative and nonoxidative mechanisms (DNA adducts), can also cause significant changes in DNA methylation (for a review see Ref.…”

Section: Discussionmentioning

confidence: 99%

“…37). Therefore, we cannot exclude that the presence of some metals in coke emissions, or rather reactive oxygen species, produced through PAH 38 or metal 36 metabolism, can contribute along with PAH exposure (for which we have supplied a measure of internal dose and biologically effective dose, i.e., the specific promutagenic anti-B[a]PDE-DNA) in modifying DNA methylation. Future work should consider the contribution of metal exposure and oxidative stress in altering DNA methylation of coke-oven workers.…”

Section: Discussionmentioning

confidence: 99%

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Global and gene‐specific promoter methylation changes are related to anti‐B[a]PDE‐DNA adduct levels and influence micronuclei levels in polycyclic aromatic hydrocarbon‐exposed individuals

Pavanello

Bollati

Pesatori

et al. 2009

Intl Journal of Cancer

137

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We investigated the effect of chronic exposure to polycyclic aromatic hydrocarbons (PAHs) on DNA methylation states (percentage of methylated cytosines (%mC)) in Polish male nonsmoking coke-oven workers and matched controls. Methylation states of gene-specific promoters (p53, p16, HIC1 and IL-6) and of Alu and LINE-1 repetitive elements, as surrogate measures of global methylation, were quantified by pyrosequencing in peripheral blood lymphocytes (PBLs). DNA methylation was evaluated in relation to PAH exposure, assessed by urinary 1-pyrenol and anti-benzo [a] We found that Alu and LINE-1 methylation levels and those of the inflammatory cytokine IL-6, to a lesser extent, were higher in polycyclic aromatic hydrocarbon (PAH)-exposed coke-oven workers than controls (p < 0.001 and p 5 0.094). Conversely, methylation of p53 and HIC1 tumor suppressors was lower in workers compared with controls (p < 0.001 and p < 0.05). Global and IL-6 hypermethylation and p53 hypomethylation were significantly correlated, not only to PAH-exposure (urinary 1-pyrenol) but also to the anti-B[a]PDE-DNA adduct levels (p < 0.01). Overall, linear multivariate regression analysis showed that the only significant determinant of increasing micronuclei (MN) (p < 0.01) was p53 hypomethylation and not the other LINE-1, Alu, p53, HIC1 and IL-6 methylation states.Gene-specific promoters (mainly p53) and global (Alu and LINE-1 repeats) DNA methylation changes in circulating peripheral blood lymphocytes (PBLs), related to anti-B[a]PDE-DNA adduct and MN, suggest that these events could be determined to identify subjects at high cancer risk.Understanding how environmental factors are involved in cancer etiology and development is one of the main goals of biomedical research. 1 Extensive research has been conducted to determine how known or potential environmental carcinogens modify the DNA sequence, as a component of malignant transformation. However, an investigative approach exclusively based on genetic damage, as well as on inheritance of genetic variants, has been revealed to be insufficient to account for multistage carcinogenic processes. 2 It has been proposed that DNA methylation, one of the best known epigenetic mechanisms, shares critical roles with DNA mutations in the theoretical continuum for exposure to cancer. 3,4 One potential mechanism for environmental factors is through hypermethylation or hypomethylation on somatic cells, leading to activation or silencing of key genes in critical pathways of cancer. 5,6 From some years, the disruption of DNA methylation status by exposure to genotoxic agents has been an issue in the literature, but the clear demonstration that such epigenetic alterations were caused by one or more specific agents in people has been demanding (for a review see Ref. 7 and references therein).Benzo [a]pyrene (B[a]P), the most well-studied PAH carcinogen (especially of the lung), has a well-established genotoxic mechanism, via metabolic activation to diol epoxide. 8 The stereoselective binding of anti-benzo[a]pyrene di...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Global and gene‐specific promoter methylation changes are related to anti‐B[a]PDE‐DNA adduct levels and influence micronuclei levels in polycyclic aromatic hydrocarbon‐exposed individuals

Pavanello

Bollati

Pesatori

et al. 2009

Intl Journal of Cancer

137

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Section: Hhs Public Accessmentioning

confidence: 99%

“…Human studies by Mills et al (2005Mills et al ( , 2007aMills et al ( , 2007b) demonstrated a dose-dependent increase in prothrombotic effects and acute myocardial ischemia upon exposure to diesel exhaust. Therefore, alternative fuels are becoming an emerging priority, as a renewable energy source that may exert reduced impacts on health (Lewtas, 2007).Over the past decade, biodiesel (BD) became an alternative energy source that is economically viable and meets requirements of the Clean Air Act. BD is a form of diesel fuel manufactured from vegetable oils, animal fats, algae, recycled restaurant greases, and other sources.…”

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confidence: 99%

Oxidative Stress, Inflammatory Biomarkers, and Toxicity in Mouse Lung and Liver after Inhalation Exposure to 100% Biodiesel or Petroleum Diesel Emissions

Shvedova

Yanamala

Murray

et al. 2013

Journal of Toxicology and Environmental Health, Part A

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Over the past decade, soy biodiesel (BD) has become a first alternative energy source that is economically viable and meets requirements of the Clean Air Act. Due to lower mass emissions and reduced hazardous compounds compared to diesel combustion emissions (CE), BD exposure is proposed to produce fewer adverse health effects. However, considering the broad use of BD and its blends in different industries, this assertion needs to be supported and validated by mechanistic and toxicological data. Here, adverse effects were compared in lungs and liver of BALB/cJ mice after inhalation exposure (0, 50, 150, or 500 μg/m 3 ; 4 h/d, 5 d/wk, for 4 wk) to CE from 100% biodiesel (B100) and diesel (D100). Compared to D100, B100 CE produced a significant accumulation of oxidatively modified proteins (carbonyls), an increase in 4-hydroxynonenal (4-HNE), a reduction of protein thiols, a depletion of antioxidant gluthatione (GSH), a dose-related rise in the levels of biomarkers of tissue damage (lactate dehydrogenase, LDH) in lungs, and inflammation (myeloperoxidase, MPO) in both lungs and liver. Significant differences in the levels of inflammatory cytokines interleukin (IL)-6, IL-10, IL-12p70, monocyte chemoattractant protein (MCP)-1, interferon (IFN) γ, and tumor necrosis factor (TNF)-α were detected in lungs and liver upon B100 and D100 CE exposures. Overall, the tissue damage, oxidative stress, inflammation, and cytokine response were more pronounced in mice exposed to Address correspondence to Dr. Anna A. Shvedova, Pathology and Physiology Research Branch (MS-2015), 1095 Willowdale Road, Morgantown, WV 26505, USA. ats1@cdc.gov. This article is not subject to U.S. copyright. Epidemiologic and occupational studies demonstrated that ambient particular matter (PM) and diesel exhaust particles exert deleterious effects on human health, including exacerbation of preexisting lung disease, increased incidence of respiratory infections, decrement in lung capacity, and enhanced risk of lung cancer (Sawyer et al., 2010;LaGier et al., 2013). According to the U.S. Environmental Protection Agency (EPA), elevated levels of airborne PM, nitrogen oxides, and sulfur oxides contribute to serious health problems in the United States, producing increased acute respiratory symptoms, chronic bronchitis, and aggravation of asthma, cardiovascular diseases, and premature mortality (Ghio et al., 2012). The International Agency for Research on Cancer (IARC) recently identified diesel combustion emissions (CE) as a Group 1 human carcinogen after chronic exposure (Benbrahim-Tallaa et al., 2012). Diesel exhaust particles are mainly aggregates of spherical carbon particles coated with inorganic and organic substances. The inorganic fraction primarily consists of small solid carbon (or elemental carbon) PM ranging from 0.01 to 0.08 microns in diameter. The organic fraction is composed of organic compounds such as aldehydes, alkanes and alkenes, and high-molecular-weight polycyclic aromatic hydrocarbons (PAH) and PAH derivatives, such as nitro-PA...

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“…Photochemical degradation is a major source of carbonyls in nature (Moortgat, 2001). Airborne carbonyls are emitted from incomplete combustion of fossil fuels in industrial plants, incinerators, automobiles and anthropogenic biomass burning (Grimaldi et al, 1995;Lewtas, 2007). Industrial resins used in manufacturing of polymeric products, such as paints and adhesives, are pollution sources as well (Fjällström et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Risk Assessment of Indoor Formaldehyde and Other Carbonyls in Campus Environments in Northwestern China

Cheng

Bai

et al. 2016

Aerosol Air Qual. Res.

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Risk assessment for indoor formaldehyde and other carbonyls was investigated at an university in Xi'an, Shaanxi, China. Eight representative locations, including six indoor workplaces and two residential units of staff apartments and a student dormitory, were chosen. The indoor pollution origins were identified according to the variability in molar composition and correlation analysis for the target species. Environmental tobacco smoke (ETS), cooking activities, and office technologies such as printers and copiers can produce different degrees of carbonyls in the workplace. A one-year demonstration study conducted in a apartment showed significance of the off-gases from lacquers and new wooden furniture. The concentrations of formaldehyde and acetaldehyde in the most sampling locations were above the recommended exposure limits, reflecting a potential health risk to workers and occupants. Chronic daily intake (CDI) and lifetime cancer hazard risk (R) were calculated to assess the carcinogenic risks of chronic exposure to the carbonyls. The R values for formaldehyde exceeded the alarm level of 1 × 10 -6 in all sampled workplaces, but lower R values were associated with acetaldehyde. The results indicate that exposure of formaldehyde is a critical occupational health and safety concern. In addition, high risks associated with formaldehyde were also measured in the staff apartment, suggesting that the refurbishing materials and wooden furniture can potentially cause health impacts to occupants. The findings are informative to be referred in establishment of indoor air quality guidelines in China.

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Air pollution combustion emissions: Characterization of causative agents and mechanisms associated with cancer, reproductive, and cardiovascular effects

Cited by 585 publications

References 327 publications

Global and gene‐specific promoter methylation changes are related to anti‐B[a]PDE‐DNA adduct levels and influence micronuclei levels in polycyclic aromatic hydrocarbon‐exposed individuals

Global and gene‐specific promoter methylation changes are related to anti‐B[a]PDE‐DNA adduct levels and influence micronuclei levels in polycyclic aromatic hydrocarbon‐exposed individuals

Oxidative Stress, Inflammatory Biomarkers, and Toxicity in Mouse Lung and Liver after Inhalation Exposure to 100% Biodiesel or Petroleum Diesel Emissions

Risk Assessment of Indoor Formaldehyde and Other Carbonyls in Campus Environments in Northwestern China

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