Human exposure to complex mixtures of air pollutants

doi:10.1016/0378-4274(94)90024-8

Toxicology Letters

Volume 72, Issues 1–3, June 1994, Pages 163-169

https://doi.org/10.1016/0378-4274(94)90024-8 Get rights and content

Abstract

Human exposure to complex mixtures of polycyclic organic matter (POM) from the products of incomplete combustion contribute to the potential lung cancer risk in urban areas. The most ubiquitous emission sources outdoors in populated areas are residential motor vehicles and residential heating, while environmental tobacco smoke is usually the major combustion source in indoor air. In addition to these urban combustion sources, there are industrial and municipal sources that may also have a significant impact on human exposure to carcinogenic agents due to their high DNA adduct and tumor initiating potency. This review focuses on new approaches to assess human exposure to POM using source apportionment, personal exposure monitoring, and biomarker methods.

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Cited by (34)

Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs)
2019, Encyclopedia of Environmental Health
Polycyclic aromatic hydrocarbons (PAH) are ubiquitous air pollutants, generated by incomplete combustion of organic material (such as gasoline and diesel fuels, coal, oil, and tobacco products). Common sources in the urban environment include traffic, particularly diesel trucks and buses, coal-fired power plants, heating fuels, and cigarette smoke. The fetus in utero and young infants are particularly vulnerable to the effects of toxicants; here we investigate the transplacental transfer as the route of exposure to PAH. Prenatal exposures to PAH have been associated with major diseases in children, including developmental disorders, asthma, and possibly cancer. All of the diseases impose significant burdens—rates of childhood asthma and developmental problems having increased in recent decades for instance. As will be discussed, synergistic interactions have been shown between these exogenous exposures and “host” factors such as genetic susceptibility and nutritional deficits.
CYP1A1 genetic polymorphism and polycyclic aromatic hydrocarbons on pulmonary function in the elderly: Haplotype-based approach for gene-environment interaction
2013, Toxicology Letters
Citation Excerpt :
Polycyclic aromatic hydrocarbons (PAHs) comprise a group of over 100 organic compounds that are formed from the incomplete burning of organic matter, such as fossil fuel and tobacco (CDC, 2009; IARC, 1983). An individual living in urban area is commonly exposed to PAHs through inhalation of outdoor air from motor vehicles, generation of electricity, and residential heating, and of indoor air from environmental tobacco smoke (ETS) (Lewtas, 1994; Nethery et al., 2012). Cooking or dietary intake of grilled meat or fish is another source of possible exposure (Viau et al., 2002).
Lung function may be impaired by environmental pollutants not only acting alone, but working with genetic factors as well. Few epidemiologic studies have been conducted to explore the interplay of polycyclic aromatic hydrocarbons (PAHs) exposure and genetic polymorphism on lung function in the elderly. For genetic polymorphism, haplotype is considered a more informative unit than single nucleotide polymorphism markers. Therefore, we examined the role of haplotype based-CYP1A1 polymorphism in the effect of PAHs exposure on lung function in 422 participants from a community-based panel of elderly adults in Seoul, Korea.
Linear mixed effect models were fit to evaluate the association of PAH exposure markers (urinary 1-hydroxypyrene and 2-naphthol) with FVC, FEV₁, FEV₁/FVC, and FEF_25–75, and then the interaction with CYP1A1 haplotype constructed from three single nucleotide polymorphisms of the gene (rs4646421/rs4646422/rs1048943).
Urinary 1-hydroxypyrene levels were inversely associated with FEV₁/FVC (p < 0.05), whereas urinary 2-naphthol levels failed to show associations with lung function. Urinary 1-hydroxypyrene was significantly associated with decrease in FEV₁/FVC among participants with rs4646421 variants (CT+TT), rs4646422 wild-type (GG), and rs1048943 wild-type (AA). At least one TGA haplotype predicted a 0.88% (95% confidence interval, 0.31–1.45%) reduction in FEV₁/FVC with an interquartile range increase in 1-hydroxypyrene, whereas no relationship was observed in participants without TGA haplotype (p for interaction = 0.045). Similar patterns were also observed in FEF_25–75. We did not find any main effects of CYP1A1 genetic polymorphisms on lung functions.
Our findings suggest that PAH exposure producing 1-hydroxypyrene as a metabolite compromises lung function in the elderly, and that haplotype-based CYP1A1 polymorphism modifies the risk.
Prenatal Exposure to Polycyclic Aromatic Hydrocarbons (PAHs)
2011, Encyclopedia of Environmental Health
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous air pollutants, generated by incomplete combustion of organic material. Common sources in the urban environment include traffic, particularly diesel trucks and buses, coal-fired power plants, heating fuels, and cigarette smoke. The fetus in utero and young infant are particularly vulnerable to the effects of toxicants. Prenatal exposures to PAHs are thought to be contributors to some major diseases in children, including developmental disorders, asthma, and cancer. All three diseases impose significant burdens – rates of childhood asthma and developmental problems having increased in recent decades. As will be discussed, synergistic interactions have been shown between these exogenous exposures and ‘host’ factors such as genetic susceptibility and nutritional deficits.
Characteristics and source identification of fine particulate n-alkanes in Beijing, China
2010, Journal of Environmental Sciences
Ambient particulate n-alkanes were determined for fine particle (PM_2.5) samples collected from Sep 2003 to July 2004 in Beijing, China. The average concentration of total n-alkanes (Σn-alkanes) from C11 to C34 was 425.72 ng/m³, ranged from 7.02 to 2893.28 ng/m³. The concentration distributions of n-alkanes homologues in this study exhibited peaks at C21 and C29 in heating season, and C29 in non-heating season. The average carbon preference index (CPI) value was 1.88 in the range of 1.18–3.88. The maximum CPI in summer indicated the contribution of biogenic origins such as plant wax; while the minimum CPI value in winter was probably a result of fossil fuel combustion. Preliminary estimation from these results showed that 59% of the n-alkanes in PM_2.5 in Beijing summer originated from plant wax, while 74%–88% was from fossil fuel combustion in other three seasons. Source estimation was further performed using principal component analysis method. Two major components were yielded accounting for 57.3% and 30.9% of the total variance, which presented the fossil fuel and biogenic contribution, respectively.
Effects of metabolic genotypes on intermediary biomarkers in subjects exposed to PAHS: Results from the EXPAH study
2007, Mutation Research - Fundamental and Molecular Mechanisms of Mutagenesis
Data from the EXPAH project on PAH exposure and intermediary biomarkers were analyzed with respect to individual genotypes at seven metabolic gene loci. The GSTM1 null allele was associated with significantly higher levels of two biomarkers, malondialdehyde-2′-deoxyguanosine and benzo[a]pyrene DNA adducts in the total population from three Central and Eastern European countries. The CYP1B1 Leu/Val variant demonstrated effects on both markers of oxidative DNA damage in opposite directions, producing a higher level of M₁dG with a trend from wild type (Leu/Leu) to heterozygotes to homozygous (Val/Val) variants, whereas the effects of these variants were reversed for 8-oxodG. Cluster Analysis was used to group composite genotypes in order to determine if combined genotypes of multiple loci could explain some of the variation seen with the biomarkers, expressed per unit of exposure, referred to as a sensitivity index. This analysis revealed two closely related genotypes each involving four of the loci (GSTM1*0/*0, CYP1A1*1*1, CYP1B1*1/*2, GSTP1*1/*1 and GSTT1*0/*0, CYP1A1*1*1, CYP1B1*1/*2, GSTP1*1/*1.) that conferred significant resistance to the DNA damaging effects of benzo[a]pyrene, measured as the level of a benzo[a]pyrene-like adduct per unit of benzo[a]pyrene exposed.
Developmental effects of exposure to environmental tobacco smoke and material hardship among inner-city children
2004, Neurotoxicology and Teratology
Because of the growing concern that exposures to airborne pollutants have adverse effects on fetal growth and early childhood neurodevelopment, and the knowledge that such exposures are more prevalent in disadvantaged populations, we assessed the joint impact of prenatal exposure to environmental tobacco smoke (ETS) and material hardship on the 2-year cognitive development of inner-city children, adjusted for other sociodemographic risks and chemical exposures. The purpose was to evaluate the neurotoxicant effects of ETS among children experiencing different degrees of socioeconomic disadvantage, within a minority population. The sample did not include children exposed to active maternal smoking in the prenatal period. Results showed significant adverse effects of prenatal residential ETS exposure and the level of material hardship on 2-year cognitive development, as well as a significant interaction between material hardship and ETS, such that children with both ETS exposure and material hardship exhibited the greatest cognitive deficit. In addition, children with prenatal ETS exposure were twice as likely to be classified as significantly delayed, as compared with nonexposed children. Postnatal ETS exposure in the first 2 years of life did not contribute independently to the risk of developmental delay, over and above the risk posed by prenatal ETS exposure. The study concluded that prenatal exposure to ETS in the home has a negative impact on 2-year cognitive development, and this effect is exacerbated under conditions of material hardship in this urban minority sample.

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Human exposure to complex mixtures of air pollutants

Abstract

Development of an exposure model for application to wintertime Boise

Complex Mixtures and Cancer Risk

Receptor models

Environ. Sci. Technol.

The contribution of wood smoke and motor vehicle emissions to ambient aerosol mutagenicitv

Environ. Sci. Technol.

Source apportionment of mutagenic activity of fine particle organics in Boise, Idaho

Complex mixtures of air pollutants: characterizing the cancer risk of polycyclic organic matter (POM)

Environ. Health Perspect.

Exposure and risk from ambient particle bound pollution in an airshed dominated by residential wood combustion and mobile sources

Environ. Health Perspec.

Biological and chemical methodologies for assessing human exposure to airborne mutagens indoors

Field test and laboratory evaluation of a lightweight, modular designed, personal sampler for human biomarker studies

IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, Polynuclear Aromatic Compounds