Association Between Individual PM2.5 Exposure and DNA Damage in Traffic Policemen

Li, Pengkun; Zhao, Jingang; Gong, Chenchen; Liang, Bo; Xie, Ying; Kan, Haidong; Song, Weimin

doi:10.1097/jom.0000000000000287

Cited by 19 publications

(6 citation statements)

References 26 publications

(23 reference statements)

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“…In fact, these mechanisms may interact to contribute to teratogenesis. For example, certain air pollutants (e.g., PM 2.5 ) could lead to genetic toxicity by forming DNA adducts (Li et al, 2014). These adducts are mutagenic, resulting in the disruption of the cell's microenvironment, which leads to inhibition of important enzymes, cell death, and alteration of other cells.…”

Section: Discussionmentioning

confidence: 99%

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

Zhou

Gilboa

Herdt

et al. 2017

Environmental Research

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Background While there is some evidence that maternal exposure to ambient air pollution is associated with orofacial clefts in offspring, the epidemiologic studies have been largely equivocal. We evaluated whether maternal exposure to elevated county-level ambient fine particulate matter with aerodynamic diameter ≤2.5 μm (PM2.5) and ozone during early gestation was associated with a higher prevalence of orofacial clefts. Methods Birth data consisting of 4.7 million births from 2001 to 2007 were obtained from National Birth Defects Prevention Network for four states — Arizona, Florida, New York (excluding New York City), and Texas. The air pollution exposure assessment for gestational weeks 5–10 was based on county-level average concentrations of PM2.5 and ozone data generated using a Bayesian fusion model available through CDC's Environmental Public Health Tracking Network. Two outcomes were analyzed separately: cleft lip with or without cleft palate, cleft palate alone. In logistic regression analyses, we adjusted for factors that were suspected confounders or modifiers of the association between the prevalence of orofacial clefts and air pollution, i.e., infant sex, race-ethnicity, maternal education, smoking status during pregnancy, whether this was mother's first baby, maternal age. Results Each 10 μg/m3 increase in PM2.5 concentration was significantly associated with cleft palate alone (OR =1.43, 95% CI: 1.11–1.86). There was no significant association between PM2.5 concentration and cleft lip with or without cleft palate. No associations were observed between ozone exposure and the two outcomes of orofacial clefts. Conclusions Our study suggests that PM2.5 significantly increased the risk of cleft palate alone, but did not change the incidence of cleft lip with or without palate. Ozone levels did not correlate with incidence of orofacial clefts.

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Section: Discussionmentioning

confidence: 99%

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

Zhou

Gilboa

Herdt

et al. 2017

Environmental Research

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“…People who work in spaces with high PM exposure (e.g., traffic attendants, street repair workers, bus drivers, etc.) may have greater exposures and thus may have increased vulnerability to PM 2.5 -induced health consequences (Han et al, 2005; Li et al, 2014). Further, the link between PM exposure and olfactory loss stresses the need for additional research into the health effects of air pollutants beyond the focus of conventional studies to date (heart, lung, and brain disease primarily), especially for sensory systems.…”

Section: Discussionmentioning

confidence: 99%

Fine particulate matter exposure and olfactory dysfunction among urban-dwelling older US adults

Ajmani

Suh

Wroblewski

et al. 2016

Environmental Research

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Objectives The olfactory nerve is anatomically susceptible to injury from pollution in inspired air, but there are no large-scale epidemiologic studies investigating this relationship. Methods Cross-sectional study using data from the National Social Life, Health, and Aging Project, a representative sample of home-dwelling US adults age 57–85 years. Olfactory function was tested using a validated 5-item odor identification test (Sniffin’ Sticks). Exposure to fine particulate matter (PM2.5) at each respondent’s home was estimated as 1–12 month moving averages prior to olfactory assessment using validated spatio-temporal models. Results Olfactory dysfunction was significantly associated with PM2.5 exposures averaged over 3–12 months in urban-dwelling respondents. The strongest effect was for 6 month average exposure (per 1-IQR increase in PM2.5: OR 1.28, 95% CI 1.05, 1.55) adjusting for age, gender, race/ethnicity, education, cognition, comorbidity, smoking, and the season. Interestingly, the most deleterious effects were observed among the youngest respondents, 57–64 years old, and those living in the northeast and south. Conclusions We show for the first time that air pollution exposure is associated with poor olfaction among urban-living, older US adults.

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“…The nematode of Caenorhabditis elegans (C. elegans), a non-mammalian model, has been widely used for biomedical and environmental toxicity evaluation because of its short lifespan, high reproduction rate, simple nervous system, adequately described genetics, high level of molecular preservation, transparent body, inexpensive and convenient maintenance, sensitivity to environmental toxins, and without the animal ethics issues (Brenner, 1973;Kaletta and Hengartner, 2006a;Leung et al, 2008;Maurer et al, 2015;Hunt, 2017;Chung et al, 2019). However, not many published articles focused on C. elegans exposure to PM2.5 and the related adverse effects, especially TRAP PM2.5 (Zhao et al, 2014;Sun et al, 2015;Yang et al, 2015;Sun et al, 2016;Wu et al, 2017;Chung et al, 2019;Zhao et al, 2019;Chung et al, 2020b). Studies on adverse effects of TRAP PM2.5 in C. elegans models, found that TRAP PM2.5 caused reproductive and neurological toxicity and shortened the lifespan of nematodes after prolonged exposure to TRAP PM2.5 (Chung et al, 2020a).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…TRAP PM2.5 has large surface areas to be covered on several organic (i.e., polycyclic aromatic hydrocarbons) or inorganic (i.e., heavy metals) chemicals and some of them are toxic (Dadvand et al, 2015;Sram et al, 2017;Rahmatinia et al, 2021;Hao et al, 2022). TRAP PM2.5 may induce inflammatory responses (Chao et al, 2018), DNA adducts or damage (Li et al, 2014), and lung function deterioration in traffic conductors or policemen (Putri Anis Syahira et al,…”

Section: Accepted Manuscript 1 Introductionmentioning

confidence: 99%

Traffic-related-air-pollutant PM2.5 Caused Toxicity on Caenorhabditis elegans with Cotreatment of High-dose Glucose and Tempeh

Tsai

Huang

et al. 2023

Aerosol Air Qual. Res.

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Rapid economic development and urbanization have significantly increased PM2.5-induced and hyperglycemia-induced toxicological effects. Tempeh is a traditional Indonesian food and may be beneficial for patients with type II diabetes. However, the toxicological effects of co-exposure to traffic-related-airpollutant (TRAP) PM2.5 with high glucose and the potential therapeutic effect of tempeh remain unclear.Using Caenorhabditis elegans (C. elegans) as an in vivo animal model, we found that exposure to 12.74 mg L -1 TRAP PM2.5 and 80 mM D-glucose could induce toxicity in nematodes that affects growth, reproduction, locomotion behavior, and lifespan. Moreover, TRAP PM2.5 and high glucose diet co-treatment reinforced these adverse effects on C. elegans. However, pretreatment with 200 µg of tempeh extract had the greatest improvement in the adverse effects of treatment with or without 12.74 mg L -1 TRAP PM2.5 and with or without 80 mM D-glucose on C. elegans. In addition, tempeh treatment also ameliorated the altered mRNA expression of the antioxidant gene in C. elegans treated with or without TRAP PM2.5 and with or without high-dose glucose diets. These findings reveal that co-exposure to TRAP PM2.5 and high-dose glucose causes more serious health effects, while tempeh could modulate oxidative stress which ameliorated TRAP PM2.5-induced and hyperglycemia-induced toxicological effects.

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Association Between Individual PM2.5 Exposure and DNA Damage in Traffic Policemen

Abstract: These results demonstrated that traffic policemen have been a high-risk group suffering DNA damage because of the high PM2.5 exposure.

Cited by 19 publications

References 26 publications

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

Maternal exposure to ozone and PM2.5 and the prevalence of orofacial clefts in four U.S. states

Fine particulate matter exposure and olfactory dysfunction among urban-dwelling older US adults

Traffic-related-air-pollutant PM2.5 Caused Toxicity on Caenorhabditis elegans with Cotreatment of High-dose Glucose and Tempeh

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