Temporal variations of fine and coarse particulate matter sources in Jeddah, Saudi Arabia.

This study provides the first comprehensive analysis of the seasonal variations and weekday/weekend differences in fine (aerodynamic diameter <2.5 µm; PM2.5) and coarse (aerodynamic diameter 2.5-10 µm; PM2.5-10) particulate matter mass concentrations, elemental constituents, and potential source origins in Jeddah, Saudi Arabia. Air quality samples were collected over 1 yr, from June 2011 to May 2012 at a frequency of three times per week, and analyzed. The average mass concentrations of PM2.5 (21.9 µg/m3) and PM10 (107.8 µg/m3) during the sampling period exceeded the recommended annual average levels by the World Health Organization (WHO) for PM2.5 (10 µg/m3) and PM10 (20 µg/m3), respectively. Similar to other Middle Eastern locales, PM2.5-10 is the prevailing mass component of atmospheric particulate matter at Jeddah, accounting for approximately 80% of the PM10 mass. Considerations of enrichment factors, absolute principal component analysis (APCA), concentration roses, and backward trajectories identified the following source categories for both PM2.5 and PM2.5-10: (1) soil/road dust, (2) incineration, and (3) traffic; and for PM2.5 only, (4) residual oil burning. Soil/road dust accounted for a major portion of both the PM2.5 (27%) and PM2.5-10 (77%) mass, and the largest source contributor for PM2.5 was from residual oil burning (63%). Temporal variations of PM2.5-10 and PM2.5 were observed, with the elevated concentration levels observed for mass during the spring (due to increased dust storm frequency) and on weekdays (due to increased traffic). The predominant role of windblown soil and road dust in both the PM2.5 and PM2.5-10 masses in this city may have implications regarding the toxicity of these particles versus those in the Western world where most PM health assessments have been made in the past. These results support the need for region-specific epidemiological investigations to be conducted and considered in future PM standard setting. IMPLICATIONS: Temporal variations of fine and coarse PM mass, elemental constituents, and sources were examined in Jeddah, Saudi Arabia, for the first time. The main source of PM2.5-10 is natural windblown soil and road dust, whereas the predominant source of PM2.5 is residual oil burning, generated from the port and oil refinery located west of the air sampler, suggesting that targeted emission controls could significantly improve the air quality in the city. The compositional differences point to a need for health effect studies to be conducted in this region, so as to directly assess the applicability of the existing guidelines to the Middle East air pollution.

Risk Assessment and Implication of Human Exposure to Road Dust Heavy Metals in Jeddah, Saudi Arabia.

Data dealing with the assessment of heavy metal pollution in road dusts in Jeddah, Saudi Arabia and its implication to human health risk of human exposure to heavy metals, are scarce. Road dusts were collected from five different functional areas (traffic areas (TA), parking areas (PA), residential areas (RA), mixed residential commercial areas (MCRA) and suburban areas (SA)) in Jeddah and one in a rural area (RUA) in Hada Al Sham. We aimed to measure the pollution levels of heavy metals and estimate their health risk of human exposure applying risk assessment models described by United States Environmental Protection Agency (USEPA). Using geo-accumulation index (Igeo), the pollution level of heavy metals in urban road dusts was in the following order Cd > As > Pb > Zn > Cu > Ni > Cr > V > Mn > Co > Fe. Urban road dust was found to be moderately to heavily contaminated with As, Pb and Zn, and heavily to extremely contaminated with Cd. Calculation of enrichment factor (EF) revealed that heavy metals in TA had the highest values compared to that of the other functional areas. Cd, As, Pb, Zn and Cu were severely enriched, while Mn, V, Co, Ni and Cr were moderately enriched. Fe was considered as a natural element and consequently excluded. The concentrations of heavy metals in road dusts of functional areas were in the following order: TA > PA > MCRA > SA > RA > RUA. The study revealed that both children and adults in all studied areas having health quotient (HQ) < 1 are at negligible non-carcinogenic risk. The only exception was for children exposed to As in TA. They had an ingestion health quotient (HQing) 1.18 and a health index (HI) 1.19. The most prominent exposure route was ingestion. The cancer risk for children and adults from exposure to Pb, Cd, Co, Ni, and Cr was found to be negligible (≤1 × 10-6).

Polycyclic aromatic hydrocarbons (PAHs) in the settled dust of automobile workshops, health and carcinogenic risk evaluation.

There are studies available on the occurrence of PAHs in indoor settled dust from residential and different occupational settings in literature but limited data is available on their occurrence and potential health risk assessment in automobile workshops. In recent decades Saudi Arabia has experienced tremendous growth in the petroleum industry and as a result, the automobile industry is booming. People working in automobile workshops are at a greater risk of exposure to chemicals releasing from the petroleum products. The main objective of this study was to report PAHs in settled dust from different automobile workshops of Jeddah, Saudi Arabia, and evaluate health risk for workers through dust exposure. Pyrene (1585-13500ng/g), Benz[a]anthracene (

Evaluation of the Effects of Airborne Particulate Matter on Bone Marrow-Mesenchymal Stem Cells (BM-MSCs): Cellular, Molecular and Systems Biological Approaches.

Particulate matter (PM) contains heavy metals that affect various cellular functions and gene expression associated with a range of acute and chronic diseases in humans. However, the specific effects they exert on the stem cells remain unclear. Here, we report the effects of PM collected from the city of Jeddah on proliferation, cell death, related gene expression and systems of biological analysis in bone marrow mesenchymal stem cells (BM-MSCs), with the aim of understanding the underlying mechanisms. PM2.5 and PM10 were tested in vitro at various concentrations (15 to 300 µg/mL) and durations (24 to 72 h). PMs induced cellular stress including membrane damage, shrinkage and death. Lower concentrations of PM2.5 increased proliferation of BM-MSCs, while higher concentrations served to decrease it. PM10 decreased BM-MSCs proliferation in a concentration-dependent manner. The X-ray fluorescence spectrometric analysis showed that PM contains high levels of heavy metals. Ingenuity Pathway Analysis (IPA) and hierarchical clustering analyses demonstrated that heavy metals were associated with signaling pathways involving cell stress/death, cancer and chronic diseases. qRT-PCR results showed differential expression of the apoptosis genes (BCL2, BAX); inflammation associated genes (TNF-α and IL-6) and the cell cycle regulation gene (p53). We conclude that PM causes inflammation and cell death, and thereby predisposes to chronic debilitating diseases.

Association between Exposure to Ambient Air Particulates and Metabolic Syndrome Components in a Saudi Arabian Population.

Recent epidemiological evidence suggests that exposure to particulates may be a factor in the etiology of metabolic syndrome (MetS). In this novel study, we investigated the relationship between particulate levels and prevalence of MetS component abnormalities (hypertension, hyperglycemia, obesity) in a recruited cohort (N = 2025) in Jeddah, Saudi Arabia. We observed significant associations between a 10 µg/m³ increase in PM2.5 and increased risks for MetS (Risk Ratio (RR): 1.12; 95% Confidence Interval (CI): 1.06-1.19), hyperglycemia (RR: 1.08; 95% CI: 1.03-1.14), and hypertension (RR: 1.09; 95% CI: 1.04-1.14). PM2.5 from soil/road dust was found to be associated with hyperglycemia (RR: 1.12; 95% CI: 1.06-1.19) and hypertension (RR: 1.11; 95% CI: 1.05-1.18), while PM2.5 from traffic was associated with hyperglycemia (RR: 1.33; 95% CI: 1.05-1.71). We did not observe any health associations with source-specific mass exposures. Our findings suggest that exposure to specific elemental components of PM2.5, especially Ni, may contribute to the development of cardiometabolic disorders.

Polycyclic aromatic hydrocarbons (PAHs) in indoor dust samples from Cities of Jeddah and Kuwait: Levels, sources and non-dietary human exposure.

This study reports levels and profiles of polycyclic aromatic hydrocarbons (PAHs) in dust samples collected from three different microenvironments (cars, air conditioner (AC) filters and household floor dust) of Jeddah, Saudi Arabia (KSA) and Kuwait. To the best of our knowledge, this is first study reporting PAHs in indoor microenvironments of KSA, which makes these findings important. Benzo(b)fluoranthene (BbF), benzo(a)pyrene (BaP), phenanthrene (Phe), and pyrene (Pyr) were found to be the major chemicals in dust samples from all selected microenvironments. ΣPAHs occurred at median concentrations (ng/g) of 3450, 2200, and 2650 in Saudi AC filter, car and household floor dust, respectively. The median levels (ng/g) of ΣPAHs in Kuwaiti car (950) and household floor (1675) dust samples were lower than Saudi dust. The PAHs profile in Saudi dust was dominated by high molecular weight (HMW) (4-5 ring) PAHs while in Kuwaiti dust 3 ring PAHs have marked contribution. BaP equivalent, a marker for carcinogenic PAHs, was high in Saudi household floor and AC filter dust with median levels (ng/g) of 370 and 455, respectively. Different exposure scenarios, using 5th percentile, median, mean, and 95th percentile levels, were estimated for adults and toddlers. For Saudi and Kuwaiti toddlers worst exposure scenario of ΣPAHs was calculated at 175 and 85ng/kg body weight/day (ng/kgbw/d), respectively. For Saudi toddlers, the calculated worst exposure scenarios for carcinogenic BaP (27.7) and BbF (29.3ng/kgbw/d) was 2-4 times higher than Kuwaiti toddlers. This study is based on small number of samples which necessitate more detailed studies for better understanding of dynamics of PAHs in the indoor environments of this region. Nevertheless, our finding supports the ongoing exposure of organic pollutants to population that accumulates indoor.

Association between sleeping hours and cardiometabolic risk factors for metabolic syndrome in a Saudi Arabian population.

OBJECTIVES: Epidemiological and molecular studies have shown that sleep duration is associated with metabolic syndrome (MtS), a disease that is on the rise in the Kingdom of Saudi Arabia. We aim to investigate the association between sleep duration and selected cardiometabolic risk factors of MtS in a Saudi Arabian population. SETTING: Secondary care was given to the participants. There were 2 participating centres, shopping malls in North and South Jeddah, Saudi Arabia. PARTICIPANTS: We recruited 2686 participants over a 1-year study period. Participants were selected based on their willingness. The only criterion for exclusion was living in the area (North or South Jeddah) for less than 15 years. PLANNED AND PRIMARY OUTCOME MEASURES: Participants were measured for blood sugar levels, blood pressure and body mass index. All participants were asked to fill out a questionnaire. RESULTS: There was a positive association between longer sleep duration and obesity, hypertension and hyperglycaemia. The adjusted ORs for obesity, hypertension and hyperglycaemia were 1.54 (95% CI 1.20 to 1.98), 1.89 (95% CI 1.45 to 2.48) and 1.59 (95% CI 1.19 to 2.13), respectively, in participants sleeping >8 h/night, as compared with those sleeping 7 h. The positive associations between longer sleep duration, defined as sleeping >7 h, and the disease status, did not differ from other risk factors such as physical activity and nutrition. CONCLUSIONS: This is the first epidemiological study reporting on the association between sleep duration and cardiometabolic risk factors of MtS in a Saudi Arabian population. Sleep durations of 8 h or greater were found to be associated with all 3 cardiometabolic risk factors: obesity, hypertension and hyperglycaemia, and this relationship was not confounded by quality of nutrition or physical activity levels.

In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes.

Particulate matter (PM) exposures have been linked to mortality, low birth weights, hospital admissions, and diseases associated with metabolic syndrome, including diabetes mellitus, cardiovascular disease, and obesity. In a previous in vitro and in vivo study, data demonstrated that PM(10µm) collected from Jeddah, Saudi Arabia (PMSA), altered expression of genes involved in lipid and cholesterol metabolism, as well as many other genes associated with metabolic disorders. PMSA contains a relatively high concentration of nickel (Ni), known to be linked to several metabolic disorders. In order to evaluate whether Ni and PM exposures induce similar gene expression profiles, mice were exposed to 100 µg/50 µl PM(SA) (PM-100), 50 µg/50 µl nickel chloride (Ni-50), or 100 µg/50 µl nickel chloride (Ni-100) twice per week for 4 wk and hepatic gene expression changes were determined. Ultimately, 55 of the same genes were altered in all 3 exposures. However, where the two Ni groups differed markedly was in the regulation (up or down) of these genes. Ni-100 and PM-100 groups displayed similar regulations, whereby 104 of the 107 genes were similarly modulated. Many of the 107 genes are involved in metabolic syndrome and include ALDH4A1, BCO2, CYP1A, CYP2U, TOP2A. In addition, the top affected pathways, such as fatty acid α-oxidation, and lipid and carbohydrate metabolism, are involved in metabolic diseases. Most notably, the top diseased outcome affected by these changes in gene expression was cardiovascular disease. Given these data, it appears that Ni and PM(SA) exposures display similar gene expression profiles, modulating the expression of genes involved in metabolic disorders.

Urinary metabolites of polycyclic aromatic hydrocarbons in Saudi Arabian schoolchildren in relation to sources of exposure.

Polycyclic aromatic hydrocarbons contain a number of known carcinogenic compounds, and urinary biomarkers have been widely used as a measure of exposure but quantitative relationships with exposure variables have proved elusive. This study aimed to quantify the relationship between exposures to phenanthrene and pyrene from atmospheric and dietary sources with the excretion of 1-hydroxypyrene and hydroxyphenanthrenes in urine as biomarkers of exposure. The study population consisted of 204 male schoolchildren attending three schools in different parts of Jeddah, Saudi Arabia who provided urine samples on each of three consecutive days. Outdoor air measurements of polycyclic aromatic hydrocarbons were made at the schools and the children provided information on diet, exposure to environmental tobacco smoke and incense, and various lifestyle factors through a questionnaire. Mixed models with random effects for subjects nested within site were fitted in order to examine the relationship between exposure variables and urinary PAH metabolites. A unit increase (1 ng m(-3)) in ambient pyrene (particulate plus gaseous phase) was associated with a 3.5% (95% CI: 1.01%, 5.13%) increase in urinary 1-hydroxypyrene concentration. A unit increase in ambient phenanthrene was associated with a 1.01% (95% CI: 0.03%, 2.02%) increase in total hydroxyphenanthrene concentrations. Consumption of chargrilled food increased the 1-hydroxypyrene and hydroxyphenanthrene concentrations by 24% (95% CI: 11%, 37%) and 17% (95% CI: 8%, 26%) respectively. We did not find evidence of association for environmental tobacco smoke exposure or incense burning. It is concluded that both respiratory exposure and consumption of chargrilled food are considerable sources of PAH exposure in this population as reflected by concentrations of urinary biomarkers.

Effects of airborne particulate matter on alternative pre-mRNA splicing in colon cancer cells.

Alternative pre-mRNA splicing plays key roles in determining tissue- and species-specific cell differentiation as well as in the onset of hereditary disease and cancer, being controlled by multiple post- and co-transcriptional regulatory mechanisms. We report here that airborne particulate matter, resulting from industrial pollution, inhibits expression and specifically affects alternative splicing at the 5' untranslated region of the mRNA encoding the bone morphogenetic protein BMP4 in human colon cells in culture. These effects are consistent with a previously reported role for BMP4 in preventing colon cancer development, suggesting that ingestion of particulate matter could contribute to the onset of colon cell proliferation. We also show that the underlying mechanism might involve changes in transcriptional elongation. This is the first study to demonstrate that particulate matter causes non-pleiotropic changes in alternative splicing.

Polycyclic aromatic hydrocarbons, brachial artery distensibility and blood pressure among children residing near an oil refinery.

BACKGROUND: Polycyclic aromatic hydrocarbons (PAH) are produced by the burning and processing of fuel oils, and have been associated with oxidant stress, insulin resistance and hypertension in adults. Few studies have examined whether adolescents are susceptible to cardiovascular effects of PAHs. OBJECTIVE: To study associations of PAH exposure with blood pressure (BP) and brachial artery distensibility (BAD), an early marker of arterial wall stiffness, in young boys attending three schools in Jeddah, Saudi Arabia in varying proximity to an oil refinery. METHODS: Air samples collected from the three schools were analyzed for PAHs. PAH metabolites (total hydroxyphenanthrenes and 1-hydroxypyrene) were measured in urine samples from 184 adolescent males, in whom anthropometrics, heart rate, pulse pressure, brachial artery distensibility and blood pressure were measured. Descriptive, bivariate and multivariable analyses were performed to assess relationships of school location and urinary PAH metabolites with cardiovascular measures. RESULTS: Total suspended matter was significantly higher (444 ± 143 µg/m(3)) at the school near the refinery compared to a school located near a ring road (395 ± 65 µg/m(3)) and a school located away from vehicle traffic (232 ± 137 µg/m(3)), as were PAHs. Systolic (0.47 S D units, p = 0.006) and diastolic (0.53 SD units, p < 0.001) BP Z-scores were highest at the school near the refinery, with a 4.36-fold increase in prehypertension (p = 0.001), controlling for confounders. No differences in pulse pressure, BAD and heart rate were noted in relationship to school location. Urinary total hydroxyphenanthrenes and 1-hydroxypyrene were not associated with cardiovascular outcomes. CONCLUSIONS: Proximity to an oil refinery in Saudi Arabia is associated with prehypertension and increases in PAH and particulate matter exposures. Further study including insulin resistance measurements, better control for confounding, and longitudinal measurement is indicated.

Receptor modelling study of polycyclic aromatic hydrocarbons in Jeddah, Saudi Arabia.

Measurements of 14 polycyclic aromatic hydrocarbons (PAH) have been made in Jeddah, Saudi Arabia, with a view to establishing the concentrations in this major city, and quantifying the contributions of major sources. Particulate and vapour forms have been sampled and analysed separately. The concentrations are compared to measurements from other sites in the Middle Eastern region and are towards the lower end of the range, being far lower than concentrations reported from Riyadh (Saudi Arabia), Assiut (Egypt) and Tehran (Iran) but broadly similar to those measured in Damascus (Syria) and higher than those measured in Kuwait. The partitioning between vapour and particle phases is similar to that in data from Egypt and China, but with many compounds showing a higher particle-associated percentage than in Birmingham (UK) possibly reflecting a higher concentration of airborne particulate matter in the former countries. Concentrations in Jeddah were significantly higher at a site close to the oil refinery and a site close to a major ring road than at a suburban site to the north of the city. Application of positive matrix factorisation to the pooled data elicited three factors accounting respectively for 17%, 33% and 50% of the measured sum of PAH and these are interpreted as arising from gasoline vehicles, industrial sources, particularly the oil refinery, and to diesel/fuel oil combustion.

Arsenic induces polyadenylation of canonical histone mRNA by down-regulating stem-loop-binding protein gene expression.

The replication-dependent histone genes are the only metazoan genes whose messenger RNA (mRNA) does not terminate with a poly(A) tail at the 3'-end. Instead, the histone mRNAs display a stem-loop structure at their 3'-end. Stem-loop-binding protein (SLBP) binds the stem-loop and regulates canonical histone mRNA metabolism. Here we report that exposure to arsenic, a carcinogenic metal, decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms. Notably, arsenic exposure dramatically increased polyadenylation of canonical histone H3.1 mRNA possibly through down-regulation of SLBP expression. The polyadenylated H3.1 mRNA induced by arsenic was not susceptible to normal degradation that occurs at the end of S phase, resulting in continued presence into mitosis, increased total H3.1 mRNA, and increased H3 protein levels. Excess expression of canonical histones have been shown to increase sensitivity to DNA damage as well as increase the frequency of missing chromosomes and induce genomic instability. Thus, polyadenylation of canonical histone mRNA following arsenic exposure may contribute to arsenic-induced carcinogenesis.

Particulate matter from Saudi Arabia induces genes involved in inflammation, metabolic syndrome and atherosclerosis.

Airborne particulate matter (PM) exposure is a major environmental health concern and is linked to metabolic disorders, such as cardiovascular diseases (CVD) and diabetes, which are on the rise in the Kingdom of Saudi Arabia. This study investigated changes in mouse lung gene expression produced by administration of PM10 collected from Jeddah, Saudi Arabia. FVB/N mice were exposed to 100 µg PM10 or water by aspiration and euthanized 24 h later. The bronchoalveolar lavage fluid (BALF) was collected and analyzed for neutrophil concentration and tumor necrosis factor (TNF)-α and interleukin (IL)-6 levels. RNA was extracted from lungs and whole transcript was analyzed using Affymetrix Mouse Gene 1.0 ST Array. Mice exposed to PM10 displayed an increase in neutrophil concentration and elevated TNF-α and IL-6 levels. Gene expression analysis revealed that mice exposed to PM10 displayed 202 genes that were significantly upregulated and 40 genes that were significantly downregulated. PM10 induced genes involved in inflammation, cholesterol and lipid metabolism, and atherosclerosis. This is the first study to demonstrate that Saudi Arabia PM10 increases in vivo expression of genes located in pathways associated with diseases involving metabolic syndrome and atherosclerosis.

Microorganisms associated particulate matter: a preliminary study.

This study aims to determine the microbiological quality of particulate matter (PM) in an urban area in Jeddah, Saudi Arabia, during December 2012 to April 2013. This was achieved by the determination of airborne bacteria, fungi, and actinobacteria associated PM10 and PM2.5, as well as their relationships with gaseous pollutants, O3, SO2 and NO2, and meteorological factors (T°C, RH% and Ws). High volume samplers with PM10 and PM2.5 selective sizes, and glass fiber filters were used to collect PM10 and PM2.5, respectively. The filters were suspended in buffer phosphate and aliquots were spread plated onto the surfaces of trypticase soy agar, malt extract agar, and starch casein agar media for counting of bacteria, fungi and actinobacteria-associated PM, respectively. PM10 and PM2.5 concentrations averaged 159.9 µg/m(3) and 60 µg/m(3), respectively, with the ratio of PM2.5/PM10 averaged ~0.4. The concentrations of O3, SO2 and NO2 averaged 35.73 µg/m(3), 38.1µg/m(3) and 52.5 µg/m(3), respectively. Fungi and actinobacteria associated PM were found in lower concentrations than bacteria. The sum of microbial loads was higher in PM10 than PM2.5, however a significant correlation (r=0.57, P ≤ 0.05) was found between the sum of microbial loads associated PM10 and PM2.5. Aspergillus fumigatus and Aspergillus niger were the common fungal types associated PM. Temperature significantly correlated with both PM10 (r=0.44), and PM2.5 (r=0.5). Significant negative correlations were found between O3 and PM2.5 (r=-0.47), and between SO2 with PM10 (r=-0.48). Wind speed positively correlated with airborne microorganisms associated PM. The regression model showed that the inverse PM2.5 concentration (1/PM2.5) was a significant determinant of fungal count associated PM. Chemical processes and environmental factors could affect properties of PM and in turn its biological quality.

Gene expression profiles in peripheral blood mononuclear cells of Chinese nickel refinery workers with high exposures to nickel and control subjects.

BACKGROUND: Occupational exposure to nickel (Ni) is associated with an increased risk of lung and nasal cancers. Ni compounds exhibit weak mutagenic activity, alter the cell's epigenetic homeostasis, and activate signaling pathways. However, changes in gene expression associated with Ni exposure have only been investigated in vitro. This study was conducted in a Chinese population to determine whether occupational exposure to Ni was associated with differential gene expression profiles in the peripheral blood mononuclear cells (PBMC) of Ni-refinery workers when compared with referents. METHODS: Eight Ni-refinery workers and ten referents were selected. PBMC RNA was extracted and gene expression profiling was conducted using Affymetrix exon arrays. Differentially expressed genes (DEG) between both groups were identified in a global analysis. RESULTS: There were a total of 2,756 DEGs in the Ni-refinery workers relative to the referents [false discovery rate (FDR) adjusted P < 0.05] with 770 upregulated genes and 1,986 downregulated genes. DNA repair and epigenetic genes were significantly overrepresented (P < 0.0002) among the DEGs. Of 31 DNA repair genes, 29 were repressed in the Ni-refinery workers and 2 were overexpressed. Of the 16 epigenetic genes, 12 were repressed in the Ni-refinery workers and 4 were overexpressed. CONCLUSIONS: The results of this study indicate that occupational exposure to Ni is associated with alterations in gene expression profiles in PBMCs of subjects. IMPACT: Gene expression may be useful in identifying patterns of deregulation that precede clinical identification of Ni-induced cancers.

Nickel and epigenetic gene silencing.

Insoluble nickel compounds are well-established human carcinogens. Occupational exposure to these compounds leads to increased incidence of lung and nasal cancer in nickel refinery workers. Apart from its weak mutagenic activity and hypoxia mimicking effect there is mounting experimental evidence indicating that epigenetic alteration plays an important role in nickel-induced carcinogenesis. Multiple epigenetic mechanisms have been identified to mediate nickel-induced gene silencing. Nickel ion is able to induce heterochromatinization by binding to DNA-histone complexes and initiating chromatin condensation. The enzymes required for establishing or removing epigenetic marks can be targeted by nickel, leading to altered DNA methylation and histone modification landscapes. The current review will focus on the epigenetic changes that contribute to nickel-induced gene silencing.

Gene expression profiling and pathway analysis of human bronchial epithelial cells exposed to airborne particulate matter collected from Saudi Arabia.

Epidemiological studies have established a positive correlation between human mortality and increased concentration of airborne particulate matters (PM). However, the mechanisms underlying PM related human diseases, as well as the molecules and pathways mediating the cellular response to PM, are not fully understood. This study aims to investigate the global gene expression changes in human cells exposed to PM(10) and to identify genes and pathways that may contribute to PM related adverse health effects. Human bronchial epithelial cells were exposed to PM(10) collected from Saudi Arabia for 1 or 4 days, and whole transcript expression was profiled using the GeneChip human gene 1.0 ST array. A total of 140 and 230 genes were identified that significantly changed more than 1.5 fold after PM(10) exposure for 1 or 4 days, respectively. Ingenuity Pathway Analysis revealed that different exposure durations triggered distinct pathways. Genes involved in NRF2-mediated response to oxidative stress were up-regulated after 1 day exposure. In contrast, cells exposed for 4 days exhibited significant changes in genes related to cholesterol and lipid synthesis pathways. These observed changes in cellular oxidative stress and lipid synthesis might contribute to PM related respiratory and cardiovascular disease.

The effect of exposure to carcinogenic metals on histone tail modifications and gene expression in human subjects.

The precise mechanisms by which nickel and arsenic compounds exert their carcinogenic properties are not completely understood. In recent years, alterations of epigenetic mechanisms have been implicated in the carcinogenesis of compounds of these two metals. In vitro exposure to certain nickel or arsenic compounds induces changes in both DNA methylation patterns, as well as, in the levels of posttranslational modifications of histone tails. Changes in DNA methylation patterns have been reported in human subjects exposed to arsenic. Here we review our recent reports on the alterations in global levels of posttranslational histone modifications in peripheral blood mononuclear cells (PBMCs) of subjects with occupational exposure to nickel and subjects exposed to arsenic in their drinking water. Occupational exposure to nickel was associated with an increase in H3K4me3 and decrease in H3K9me2. A global increase in H3K9me2 and decrease in H3K9ac was found in subjects exposed to arsenic. Additionally, exposure to arsenic resulted in opposite changes in a number of histone modifications in males when compared with females in the arsenic population. The results of these two studies suggest that exposure to nickel or arsenic compounds, and possibly other carcinogenic metal compounds, can induce changes in global levels of posttranslational histone modifications in peripheral blood mononuclear cells.

Source Apportionment and Elemental Composition of PM2.5 and PM10 in Jeddah City, Saudi Arabia.

This paper presents the first comprehensive investigation of PM2.5 and PM10 composition and sources in Saudi Arabia. We conducted a multi-week multiple sites sampling campaign in Jeddah between June and September, 2011, and analyzed samples by XRF. The overall mean mass concentration was 28.4 ± 25.4 µg/m3 for PM2.5 and 87.3 ± 47.3 µg/m3 for PM10, with significant temporal and spatial variability. The average ratio of PM2.5/PM10 was 0.33. Chemical composition data were modeled using factor analysis with varimax orthogonal rotation to determine five and four particle source categories contributing significant amount of for PM2.5 and PM10 mass, respectively. In both PM2.5 and PM10 sources were (1) heavy oil combustion characterized by high Ni and V; (2) resuspended soil characterized by high concentrations of Ca, Fe, Al, and Si; and (3) marine aerosol. The two other sources in PM2.5 were (4) Cu/Zn source; (5) traffic source identified by presence of Pb, Br, and Se; while in PM10 it was a mixed industrial source. To estimate the mass contributions of each individual source category, the CAPs mass concentration was regressed against the factor scores. Cumulatively, resuspended soil and oil combustion contributed 77 and 82% mass of PM2.5 and PM10, respectively.