科研成果

Background: More than 90% of the world's population lives in areas where outdoor air pollution levels exceed health-based limits. In these areas, individuals may use indoor air filtration, often on a sporadic basis, in their residences to reduce exposure to respirable particles (PM2.5). Whether this intervention can lead to improvements in health outcomes has not been evaluated.Methods: Seventy non-smoking healthy adults, aged 19 to 26 years, received both true and sham indoor air filtration in a double-blinded randomized crossover study. Each filtration session was approximately 13 h long. True and sham filtration sessions were separated by a two-week washout interval. The study was carried out in a suburb of Shanghai.Results: During the study period, outdoor PM2.5 concentrations ranged from 18.6 to 106.9 mu g/m(3), which overlapped with levels measured in Western Europe and North America. Compared to sham filtration, true filtration on average decreased indoor PM2.5 concentration by 72.4% to 10.0 mu g/m(3) and particle number concentration by 59.2% to 2316/cm(3). For lung function measured immediately after the end of filtration, true filtration significantly lowered airway impedance at 5 Hz (Z(5)) by 7.1% [95% CI: 2.4%, 11.9%], airway resistance at 5 Hz (R-5) by 7.4% [95% CI: 2.4%, 12.5%], and small airway resistance (R-5-R-20) by 20.3% [95% CI: 0.1%, 40.5%], reflecting improved airway mechanics especially for the small airways. However, no significant improvements for spirometry indicators (FEV1, FVC) were observed. True filtration also significantly lowered von Willebrand factor (VWF) by 26.9% [95% CI: 7.3%, 46.4%] 24 h after the end of filtration, indicating reduced risk for thrombosis. Stratified analysis in male and female participants showed that true filtration significantly decreased pulse pressure by 3.3% [95% CI: 0.8%, 7.4%] in females, and significantly reduced VWF by 42.4% [95% CI: 17.4%, 67.4%] and interleukin-6 by 22.6% [95% CI: 0.4%, 44.9%] in males. Effect modification analyses indicated that filtration effects in male and female participants were not significantly different.Conclusion: A single overnight residential air filtration, capable of reducing indoor particle concentrations substantially, can lead to improved airway mechanics and reduced thrombosis risk.

High-efficiency particulate air (HEPA) filtration in combination with an electrostatic precipitator (ESP) can be a cost-effective approach to reducing indoor particulate exposure, but ESPs produce ozone. The health effect of combined ESP-HEPA filtration has not been examined. We conducted an intervention study in 89 volunteers. At baseline, the air-handling units of offices and residences for all subjects were comprised of coarse, ESP, and HEPA filtration. During the 5-week long intervention, the subjects were split into 2 groups, 1 with just the ESP removed and the other with both the ESP and HEPA removed. Each subject was measured for cardiopulmonary risk indicators once at baseline, twice during the intervention, and once 2 weeks after baseline conditions were restored. Measured indoor and outdoor PM2.5 and ozone concentrations, coupled with time-activity data, were used to calculate exposures. Removal of HEPA filters increased 24-hour mean PM2.5 exposure by 38 (95% CI: 31, 45) mug/m(3) . Removal of ESPs decreased 24-hour mean ozone exposure by 2.2 (2.0, 2.5) ppb. No biomarkers were significantly associated with HEPA filter removal. In contrast, ESP removal was associated with a -16.1% (-21.5%, -10.4%) change in plasma-soluble P-selectin and a -3.0% (-5.1%, -0.8%) change in systolic blood pressure, suggesting reduced cardiovascular risks.

Background: Oxidative stress is involved in thoracic diseases and health responses to air pollution. Malondialdehyde (MDA) is a well-established marker of oxidative stress, but it may be present in unconjugated and conjugated forms. To our knowledge, no studies have conducted a systemic evaluation of both free MDA (unconjugated MDA) and total MDA (the sum of both unconjugated and conjugated MDA) across various types of human biospecimens.Methods: Free MDA and total MDA were simultaneously measured in a range of human biospecimens, including nasal fluid (N=158), saliva (N=158), exhaled breath condensate (N=40), serum (N=232), and urine (N=429). All samples were analyzed using an HPLC-fluorescence method with high sensitivity and specificity. Due to the right skewed distribution of free MDA and total MDA, we performed natural-log transformation before subsequent statistical analyses. The relationship between the natural log of free and total MDA was evaluated by R-2 of simple linear regression. T test was used for comparisons of means between two groups. One-way analysis of variance was used in combination with Tukey's test to compare the natural log of the ratio of free MDA to total MDA across various types of biospecimens.Results: For exhaled breath condensate, serum, urine, nasal fluid and saliva samples, the R-2 between free and total MDA were 0.61, 0.22, 0.59, 0.47 and 0.06, respectively; the medians of the free MDA to total MDA ratio were 48.1%, 17.4%, 9.8%, 5.1% and 3.0%, respectively; the free MDA to total MDA ratio in EBC > serum > urine > nasal fluid > saliva (P < 0.001 for pairwise comparisons).Conclusions: For exhaled breath condensate and urine samples, using either free or total MDA can provide information regarding the level of oxidative stress; however, that is not the case for serum, nasal fluid, and saliva given the low correlations between free and total MDA.

Polycyclic aromatic hydrocarbons (PAH) are ubiquitous air pollutants associated with negative impacts on growth, development and behavior in children. Source-specific biological markers of PAH exposure are needed for targeting interventions to protect children. Nitro-derivatives of PAH can act as markers of exposure to diesel exhaust, gasoline exhaust, or general combustion sources. Using a novel HPLC-APCI-MS/MS detection method, we examined four hemoglobin (Hb) adducts of nitro-PAH metabolites and the Hb adduct of a benzo[a]pyrene (BaP) metabolite in 22 umbilical cord blood samples. The samples were collected from a birth cohort with comprehensive data on prenatal PAH exposure, including prenatal personal air monitoring and DNA adducts in maternal and umbilical cord blood. Using non-parametric analyses, heat maps, and principal component analysis (PCA), we analyzed the relationship between the five Hb adducts and previous PAH measurements, with each measurement representing a different duration of exposure. We found that Hb adducts derived from several diesel-related nitro-PAHs (2-nitrofluorene and 1-nitropyrene) were significantly correlated (r = 0.77, p

OBJECTIVES: We assessed relationships between indoor black carbon (BC) exposure and urinary oxidative stress biomarkers, 8-hydroxy-2'-deoxyguanosine (8-OHdG) and malondialdehyde (MDA), in participants with chronic obstructive pulmonary disease (COPD). METHODS: Eighty-two participants completed in-home air sampling for one week prior to providing urine samples up to four times in a year. Weekly indoor and daily outdoor concentrations were used to estimate indoor daily lags and moving averages. There were no reported in-home BC sources, thus indoor levels closely represented outdoor BC infiltration. Mixed effects regression models with a random intercept for each participant were used to assess relationships between indoor BC and 8-OHdG and MDA, adjusting for age, race, BMI, diabetes, heart disease, season, time of urine collection, urine creatinine, and outdoor humidity and temperature. RESULTS: There were positive effects of BC on 8-OHdG and MDA, with the greatest effect the day before urine collection (6.9% increase; 95% CI 0.9-13.3%, per interquartile range: 0.22mug/m(3)) for 8-OHdG and 1 to 4days before collection (8.3% increase; 95% CI 0.03-17.3% per IQR) for MDA. Results were similar in models adjusting for PM2.5 not associated with BC and NO2 (10.4% increase, 95% CI: 3.5-17.9 for 8-OHdG; 8.1% increase, 95% CI: -1.1-18.1 for MDA). Effects on 8-OHdG were greater in obese participants. CONCLUSIONS: We found positive associations between BC exposure and 8-OHdG and MDA, in which associations with 8-OHdG were stronger in obese participants. These results suggest that exposure to low levels of traffic-related pollution results in lipid peroxidation and oxidative DNA damage in individuals with COPD.

BACKGROUND: Long-term exposure to pollution can lead to an increase in the rate of decline of lung function, especially in older individuals and in those with chronic obstructive pulmonary disease (COPD), whereas shorter-term exposure at higher pollution levels has been implicated in causing excess deaths from ischaemic heart disease and exacerbations of COPD. We aimed to assess the effects on respiratory and cardiovascular responses of walking down a busy street with high levels of pollution compared with walking in a traffic-free area with lower pollution levels in older adults. METHODS: In this randomised, crossover study, we recruited men and women aged 60 years and older with angiographically proven stable ischaemic heart disease or stage 2 Global initiative for Obstructive Lung Disease (GOLD) COPD who had been clinically stable for 6 months, and age-matched healthy volunteers. Individuals with ischaemic heart disease or COPD were recruited from existing databases or outpatient respiratory and cardiology clinics at the Royal Brompton & Harefield NHS Foundation Trust and age-matched healthy volunteers using advertising and existing databases. All participants had abstained from smoking for at least 12 months and medications were taken as recommended by participants' doctors during the study. Participants were randomly assigned by drawing numbered disks at random from a bag to do a 2 h walk either along a commercial street in London (Oxford Street) or in an urban park (Hyde Park). Baseline measurements of participants were taken before the walk in the hospital laboratory. During each walk session, black carbon, particulate matter (PM) concentrations, ultrafine particles, and nitrogen dioxide (NO2) concentrations were measured. FINDINGS: Between October, 2012, and June, 2014, we screened 135 participants, of whom 40 healthy volunteers, 40 individuals with COPD, and 39 with ischaemic heart disease were recruited. Concentrations of black carbon, NO2, PM10, PM2.5, and ultrafine particles were higher on Oxford Street than in Hyde Park. Participants with COPD reported more cough (odds ratio [OR] 1.95, 95% CI 0.96-3.95; p<0.1), sputum (3.15, 1.39-7.13; p<0.05), shortness of breath (1.86, 0.97-3.57; p<0.1), and wheeze (4.00, 1.52-10.50; p<0.05) after walking down Oxford Street compared with Hyde Park. In all participants, irrespective of their disease status, walking in Hyde Park led to an increase in lung function (forced expiratory volume in the first second [FEV1] and forced vital capacity [FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk. By contrast, these beneficial responses were attenuated after walking on Oxford Street. In participants with COPD, a reduction in FEV1 and FVC, and an increase in R5-20 were associated with an increase in during-walk exposure to NO2, ultrafine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles. In healthy volunteers, PWV and augmentation index were associated both with black carbon and ultrafine particles. INTERPRETATION: Short-term exposure to traffic pollution prevents the beneficial cardiopulmonary effects of walking in people with COPD, ischaemic heart disease, and those free from chronic cardiopulmonary diseases. Medication use might reduce the adverse effects of air pollution in individuals with ischaemic heart disease. Policies should aim to control ambient levels of air pollution along busy streets in view of these negative health effects. FUNDING: British Heart Foundation.

Importance: Exposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood. Objective: To examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms. Design, Setting, and Participants: A longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates. Main Outcomes and Measures: Biomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions. Results: Of the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a -9.5% (95% CI, -17.7% to -1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures. Conclusions and Relevance: Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.

OBJECTIVES: We previously reported that compared with night sleep, day sleep among shift workers was associated with reduced urinary excretion of 8-hydroxydeoxyguanosine (8-OH-dG), potentially reflecting a reduced ability to repair 8-OH-dG lesions in DNA. We identified the absence of melatonin during day sleep as the likely causative factor. We now investigate whether night work is also associated with reduced urinary excretion of 8-OH-dG. METHODS: For this cross-sectional study, 50 shift workers with the largest negative differences in night work versus night sleep circulating melatonin levels (measured as 6-sulfatoxymelatonin in urine) were selected from among the 223 shift workers included in our previous study. 8-OH-dG concentrations were measured in stored urine samples using high performance liquid chromatography with electrochemical detection. Mixed effects models were used to compare night work versus night sleep 8-OH-dG levels. RESULTS: Circulating melatonin levels during night work (mean=17.1 ng/mg creatinine/mg creatinine) were much lower than during night sleep (mean=51.7 ng/mg creatinine). In adjusted analyses, average urinary 8-OH-dG levels during the night work period were only 20% of those observed during the night sleep period (95% CI 10% to 30%; p<0.001). CONCLUSIONS: This study suggests that night work, relative to night sleep, is associated with reduced repair of 8-OH-dG lesions in DNA and that the effect is likely driven by melatonin suppression occurring during night work relative to night sleep. If confirmed, future studies should evaluate melatonin supplementation as a means to restore oxidative DNA damage repair capacity among shift workers.

Using data collected before, during, and after the 2008 Summer Olympic Games in Beijing, this study examines associations between biomarkers of blood coagulation (vWF, sCD62P and sCD40L), pulmonary inflammation (EBC pH, EBC nitrite, and eNO), and systemic oxidative stress (urinary 8-OHdG) with sources of air pollution identified utilizing principal component analysis and with concentrations of three aldehydes of health concern. Associations between the biomarkers and the air pollution source types and aldehydes were examined using a linear mixed effects model, regressing through seven lag days and controlling for ambient temperature, relative humidity, gender, and day of week for the biomarker measurements. The biomarkers for pulmonary inflammation, particularly EBC pH and eNO, were most consistently associated with vehicle and industrial combustion, oil combustion, and vegetative burning. The biomarkers for blood coagulation, particularly vWF and sCD62p, were most consistently associated with oil combustion. Systemic oxidative stress biomarker (8-OHdG) was most consistently associated with vehicle and industrial combustion. The associations of the biomarkers were generally not significant or consistent with secondary formation of pollutants and with the aldehydes. The findings support policies to control anthropogenic pollution sources rather than natural soil or road dust from a cardio-respiratory health standpoint.

There is a potential for silver nanowires (AgNWs) to be inhaled, but there is little information on their health effects and their chemical transformation inside the lungs in vivo. We studied the effects of short (S-AgNWs; 1.5 mum) and long (L-AgNWs; 10 mum) nanowires instilled into the lungs of Sprague-Dawley rats. S- and L-AgNWs were phagocytosed and degraded by macrophages; there was no frustrated phagocytosis. Interestingly, both AgNWs were internalized in alveolar epithelial cells, with precipitation of Ag2S on their surface as secondary Ag2S nanoparticles. Quantitative serial block face three-dimensional scanning electron microscopy showed a small, but significant, reduction of NW lengths inside alveolar epithelial cells. AgNWs were also present in the lung subpleural space where L-AgNWs exposure resulted in more Ag+ve macrophages situated within the pleura and subpleural alveoli, compared with the S-AgNWs exposure. For both AgNWs, there was lung inflammation at day 1, disappearing by day 21, but in bronchoalveolar lavage fluid (BALF), L-AgNWs caused a delayed neutrophilic and macrophagic inflammation, while S-AgNWs caused only acute transient neutrophilia. Surfactant protein D (SP-D) levels in BALF increased after S- and L-AgNWs exposure at day 7. L-AgNWs induced MIP-1alpha and S-AgNWs induced IL-18 at day 1. Large airway bronchial responsiveness to acetylcholine increased following L-AgNWs, but not S-AgNWs, exposure. The attenuated response to AgNW instillation may be due to silver inactivation after precipitation of Ag2S with limited dissolution. Our findings have important consequences for the safety of silver-based technologies to human health.

Nanoceria (i.e., CeO2 nanoparticles) fuel additives have been used in Europe and elsewhere to improve fuel efficiency. Previously we have shown that the use of a commercial fuel additive Envirox in a diesel-powered electricity generator reduced emissions of diesel exhaust particle (DEP) mass and other pollutants. However, such additives are currently not permitted for use in on-road vehicles in North America, largely due to limited data on the potential health impact. In this study, we characterized a variety of physicochemical properties of DEPs emitted from the same engine. Our methods include novel techniques such as Raman spectrometry for analyzing particle surface structure and an assay for DEP oxidative potential. Results show that with increasing Envirox concentrations in the fuel (0x, 0.1x, 1x, and 10x of manufacturer recommended 0.5 mL Envirox per liter fuel), DEP sizes decreased from 194.6 +/- 20.1 to 116.3 +/- 14.8 nm; the zeta potential changed from -28.4 mV to -22.65 mV; DEP carbon content decreased from 91.8% to 79.4%; cerium and nitrogen contents increased from 0.3% to 6.5% and 0.2% to 0.6%, respectively; the ratio of organic carbon (OC) to elemental carbon (EC) increased from 22.9% to 38.7%; and the ratio of the disordered carbon structure to the ordered carbon structure (graphitized carbon) in DEPs decreased. Compared to DEPs emitted from 0x, 0.1x, and 1x fuels, DEPs from the 10x fuel had a lower oxidative potential likely due to the increased ceria content because pure ceria nanoparticles exhibited the lowest oxidative potential compared to all the DEPs. Since the physicochemical parameters tested here are among the determinants of particle toxicity, our findings imply that adding ceria nanoparticles into diesel may alter the toxicity of DEPs. The findings from the present study, hence, can help future studies that will examine the impact of nanoceria additives on DEP toxicities.

BACKGROUND: The increasing use of silver nanoparticles (AgNPs) in consumer products is concerning. We examined the potential toxic effects when inhaled in Brown-Norway (BN) rats with a pre-inflammatory state compared to Sprague-Dawley (SD) rats. METHODS: We determined the effect of AgNPs generated from a spark generator (mass concentration: 600-800 mug/mm(3); mean diameter: 13-16 nm; total lung doses: 8 [Low] and 26-28 [High] mug) inhaled by the nasal route in both rat strains. Rats were sacrificed at day 1 and day 7 after exposure and measurement of lung function. RESULTS: In both strains, there was an increase in neutrophils in bronchoalveolar lavage (BAL) fluid at 24 h at the high dose, with concomitant eosinophilia in BN rats. While BAL inflammatory cells were mostly normalised by Day 7, lung inflammation scores remained increased although not the tissue eosinophil scores. Total protein levels were elevated at both lung doses in both strains. There was an increase in BAL IL-1beta, KC, IL-17, CCL2 and CCL3 levels in both strains at Day 1, mostly at high dose. Phospholipid levels were increased at the high dose in SD rats at Day 1 and 7, while in BN rats, this was only seen at Day 1; surfactant protein D levels decreased at day 7 at the high dose in SD rats, but was increased at Day 1 at the low dose in BN rats. There was a transient increase in central airway resistance and in tissue elastance in BN rats at Day 1 but not in SD rats. Positive silver-staining was seen particularly in lung tissue macrophages in a dose and time-dependent response in both strains, maximal by day 7. Lung silver levels were relatively higher in BN rat and present at day 7 in both strains. CONCLUSIONS: Presence of cellular inflammation and increasing silver-positive macrophages in lungs at day 7, associated with significant levels of lung silver indicate that lung toxicity is persistent even with the absence of airway luminal inflammation at that time-point. The higher levels and persistence of lung silver in BN rats may be due to the pre-existing inflammatory state of the lungs.

Hydrogen sulfide (H2S), a novel signaling gasotransmitter in the respiratory system, may have antiinflammatory properties in the lung. We examined the preventive and therapeutic effects of H2S on ozone-induced features of lung inflammation and emphysema. C57/BL6 mice were exposed to ozone or filtered air over 6 weeks. Sodium hydrogen sulfide (NaHS), an H2S donor, was administered to the mice either before ozone exposure (preventive effect) or after completion of 6 weeks of ozone exposure (therapeutic effect). The ozone-exposed mice developed emphysema, measured by micro-computed tomography and histology, airflow limitation, measured by the forced maneuver system, and increased lung inflammation with augmented IL-1beta, IL-18, and matrix metalloproteinase-9 (MMP-9) gene expression. Ozone-induced changes were associated with increased Nod-like receptor pyrin domain containing 3 (NLRP3)-caspase-1 activation and p38 mitogen-activated protein kinase phosphorylation and decreased Akt phosphorylation. NaHS both prevented and reversed lung inflammation and emphysematous changes in alveolar space. In contrast, NaHS prevented, but did not reverse, ozone-induced airflow limitation and bronchial structural remodeling. In conclusion, NaHS administration prevented and partially reversed ozone-induced features of lung inflammation and emphysema via regulation of the NLRP3-caspase-1, p38 mitogen-activated protein kinase, and Akt pathways.

Dietary intake is one of the major exposure pathways of polycyclic aromatic hydrocarbons (PAHs), especially in Chinese people because foods are often prepared with grilling and/or frying that would produce high levels of PAHs. In this paper, we assessed daily dietary intakes (DDI) of PAHs, using a "duplicate plate method", among 100 Chinese urban residents. The DDI of benzo(a)pyrene ranged from 0.06 mu g per day to 13.5 mu g per day with a median of 0.69 mu g per day, varying largely across subjects. The median Incremental Lifetime Cancer Risk (ILCR) attributable to PAH dietary intake was 6.65 x 10(-5) (4.41 x 10(-5) to 1.02 x 10(-4) as inter-quartile range). The contribution of several high-PAH containing foods like barbecued, smoked or deep-fried meats to the overall DDIs was about 13%. The use of raw foods may underestimate dietary intake of PAHs and associated exposure risk considerably. Results from foods sampled in different seasons suggested that seasonal variability within an individual may contribute notably to overall variability measured in a population and more future studies with longer-term investigation on food ingestion and pollutant exposure are needed. The study indicates that measuring actually consumed foods is more appropriate for dietary intake exposure assessment, and intra-individual variance should be taken into account during study design and data analysis. (C) 2015 Elsevier Ltd. All rights reserved.

Objectives Oxidative DNA damage may be increased among nightshift workers because of suppression of melatonin, a cellular antioxidant, and/or inflammation related to sleep disruption. However, oxidative DNA damage has received limited attention in previous studies of nightshift work.Methods From two previous cross-sectional studies, urine samples collected during a night sleep period for 217 dayshift workers and during day and night sleep (on their first day off) periods for 223 nightshift workers were assayed for 8-hydroxydeoxyguanosine (8-OH-dG), a marker of oxidative DNA damage, using high-performance liquid chromatography with electrochemical detection. Urinary measures of 6-sulfatoxymelatonin (aMT6s), a marker of circulating melatonin levels, and actigraphy-based sleep quality data were also available.Results Nightshift workers during their day sleep periods excreted 83% (p=0.2) and 77% (p=0.03) of the 8-OH-dG that dayshift workers and they themselves, respectively, excreted during their night sleep periods. Among nightshift workers, higher aMT6s levels were associated with higher urinary 8-OH-dG levels, and an inverse U-shaped trend was observed between 8-OH-dG levels and sleep efficiency and sleep duration.Conclusions Reduced excretion of 8-OH-dG among nightshift workers during day sleep may reflect reduced functioning of DNA repair machinery, which could potentially lead to increased cellular levels of oxidative DNA damage. Melatonin disruption among nightshift workers may be responsible for the observed effect, as melatonin is known to enhance repair of oxidative DNA damage. Quality of sleep may similarly impact DNA repair. Cellular levels of DNA damage will need to be evaluated in future studies to help interpret these findings.