Pervasiveness, bioaccumulation and subduing environmental health challenges posed by polycyclic aromatic hydrocarbons (PAHs): A systematic review to settle a one health strategy in Niger Delta, Nigeria.

The crude oil-rich Niger Delta region of Nigeria is under threat due to anthropogenic activities that include mainly PAH contamination. Following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), multiple online searches were conducted using several databases (e.g. Cochrane Library, Scopus, Embase, National Library of Medicine, PubMed etc.) between October and November 2022 to collect evidence on pervasiveness, bioaccumulation and health challenges posed by PAH in Nigeria Niger Delta. Included studies were appraised for quality using the Standard for Quality Improvement Reporting Excellence (SQUIRE 2.0) framework and the Joanna Briggs (JB) checklist and retrieved data were analysed using the narrative synthesis method. With the indiscriminate exposure of the local inhabitants to PAH and a lack of public health policies that efficiently prevent exposure-associated adverse health events, there is a need for a collaborative and multi-disciplinary approach, cutting across boundaries of animal, human, and environmental health to undertake risk assessments, develop plans for response and control in an attempt to protect public health. The complex and wide distribution of PAHs within the Niger Delta region would benefit of the One Health strategy. Such systemic approach would help managing the harmful effects of PAHs on ecosystems, from environmental remedial approaches to measures to mitigate exposure-associated risks. One health, including environmental health and food safety, would help risk assessors and risk managers in prioritising actions for the prevention and mitigation of PAHs pollution and its spread and accumulation.

Urinary PAHs metabolites in Karakoram Highway's heavy traffic vehicle (HTV) drivers: evidence of exposure and health risk.

The current study features PAHs exposure on Karakoram Highway, a route of utmost importance in Pakistan. The drivers of heavy traffic vehicles (HTV) on Karakoram Highway spend long hours amid dense traffic and therefore, inevitably inhale huge amount of PAH carcinogens. The urinary metabolites of PAHs in such drivers (meeting selection criteria n = 48) and a control group (n = 49) were comparatively profiled. The higher urinary biomarkers among ninety-six percent HTV drivers were evident of PAHs exposure. We observed elevated concentrations of urinary benzo[a]pyrene metabolites (3-OH-BaP = 3.53 ± 0.62 ng g-1 creatinine and 9-OH-BaP = 3.69 ± 0.74 ng g-1 creatinine) in HTV driver's samples compared to controls (0.85 ± 0.08 and 0.31 ± 0.03 ng g-1 creatinine, respectively). Interestingly, urinary benzo[a]pyrene metabolites were detected in almost similar amount among HTV drivers irrespective of their working hours. A distinct smoking effect was manifested with rising urinary levels of 1-hydroxypyrene, 2-hydroxyphenanthrene, and 3-hydroxybenzo[a]pyrene with corresponding increase in driving hours per day. These metabolites exhibited characteristic exposures to low molecular weight volatile PAHs that are commonly found in vehicular exhaust. The elevated PAH body burden was directly linked to the nature of their job and the route-long environmental pollution on Karakoram Highway. Additionally, the poor economic status and smoking also increased HTV driver's health vulnerability and significantly declined their health capacity. There was conclusive evidence that HTV drivers were exposed to PAHs during a ride on Karakoram Highway, back and forth, an aspect not reported earlier.

Wildfire Impact on Indoor and Outdoor PAH Air Quality.

Air quality impacts from wildfires are poorly understood, particularly indoors. As frequencies increase, it is important to optimize methodologies to understand and reduce chemical exposures from wildfires. Public health recommendations use air quality estimates from outdoor stationary air monitors, discounting indoor air conditions, and do not consider chemicals in the vapor phase, known to elicit adverse effects. We investigated vapor-phase polycyclic aromatic hydrocarbons (PAHs) in indoor and outdoor air before, during, and after wildfires using a community-engaged research approach. Paired passive air samplers were deployed at 15 locations across four states. Twelve unique PAHs were detected only in outdoor air during wildfires, highlighting a PAH exposure mixture for future study. Heavy-molecular-weight (HMW) outdoor PAH concentrations and average Air Quality Index (AQI) values were positively correlated (p < 0.001). Indoor PAH concentrations were higher in 77% of samples across all sampling events. Even during wildfires, 58% of sampled locations still had higher indoor PAH air concentrations. When AQI values exceeded 140 (unhealthy for sensitive groups), outdoor PAH concentrations became similar to or higher than indoors. Cancer and noncancer inhalation risk estimates from vapor-phase PAHs were higher indoors than outdoors, regardless of the wildfire impact. Consideration of indoor air quality and vapor-phase PAHs could inform public health recommendations regarding wildfires.

Individual and Combined Effects of Environmental Risk Factors for Esophageal Cancer Based on Results From the Golestan Cohort Study.

BACKGROUND & AIMS: Northeast Iran has one of the highest reported rates of esophageal squamous cell carcinoma (ESCC) worldwide. Decades of investigations in this region have identified some local habits and environmental exposures that increase risk. We analyzed data from the Golestan Cohort Study to determine the individual and combined effects of the major environmental risk factors of ESCC. METHODS: We performed a population-based cohort of 50,045 individuals, 40 to 75 years old, from urban and rural areas across Northeast Iran. Detailed data on demographics, diet, lifestyle, socioeconomic status, temperature of drinking beverages, and different exposures were collected using validated methods, questionnaires, and physical examinations, from 2004 through 2008. Participants were followed from the date of enrollment to the date of first diagnosis of esophageal cancer, date of death from other causes, or date of last follow-up, through December 31, 2017. Proportional hazards regression models were used to estimate hazard ratios (HRs) and corresponding 95% confidence intervals (CIs) for the association between different exposures and ESCC. RESULTS: During an average 10 years of follow-up, 317 participants developed ESCC. Opium smoking (HR 1.85; 95% CI 1.18-2.90), drinking hot tea (≥60°C) (HR 1.60; 95% CI 1.15-2.22), low intake of fruits (HR 1.48; 95% CI 1.07-2.05) and vegetables (HR 1.62; 95% CI 1.03-2.56), excessive tooth loss (HR 1.66; 95% CI 1.04-2.64), drinking unpiped water (HR 2.04; 95% CI 1.09-3.81), and exposure to indoor air pollution (HR 1.57; 95% CI 1.08-2.29) were significantly associated with increased risk of ESCC, in a dose-dependent manner. Combined exposure to these risk factors was associated with a stepwise increase in the risk of developing ESCC, reaching a more than 7-fold increase in risk in the highest category. Approximately 75% of the ESCC cases in this region can be attributed to a combination of the identified exposures. CONCLUSIONS: Analysis of data from the Golestan Cohort Study in Iran identified multiple risk factors for ESCC in this population. Our findings support the hypothesis that the high rates of ESCC are due to a combination of factors, including thermal injury (from hot tea), exposure to polycyclic aromatic hydrocarbons (from opium and indoor air pollution), and nutrient-deficient diets. We also associated ESCC risk with exposure to unpiped water and tooth loss.

PAH concentrations and exposure assessment from house dust retained in air-conditioning filters collected from Greater Doha, Qatar.

Polycyclic aromatic hydrocarbons (PAHs) bound in dust retained in air-conditioning unit filters from 13 households in Greater Doha, Qatar, were quantified using GC-MS spectrometry. The median concentrations of ∑16PAH and ∑7PAH were 218.0 ng g-1 (± 125.3) and 112.1 ng g-1 (± 60.2) dry weight, respectively. Results show that except one sample, three- and four-benzene-ring PAHs were dominant in all dust samples. Phenanthrene, anthracene, pyrene, benzene(a)anthracene, and chrysene were dominant in 12 samples with maximum concentrations of 69.7 ng g-1 (± 24.0), 92.9 ng g-1 (± 28.1), 60.4 ng g-1 (± 14.7), 38.6 ng g-1 (± 7.3), and 14.7 ng g-1 (± 3.5), respectively. Benzo(k)fluoranthene has the most abundance of the quantified PAHs in the dust samples accounting for 19% of the total PAHs. Although Kriging interpolation shows a spatial variation of PAHs from north to south of Greater Doha, the mean concentrations in both directions were statically insignificant. Five samples displayed levels of benzo(a)pyrene (BaP) with maximum and median concentrations at 110.8 ng g-1 and 49.9 (± 28.4) dry weight, respectively. Benzo(a)pyrene equivalent approach [Formula: see text] was applied to assess carcinogenic exposure, and the resulting values (1.3-116.4 ng g-1) indicate that the levels observed were below the values reported for other countries within the region. Estimated daily ingestion (EDI) rates of PAHs retained in ACU filters were assessed for five age-groups < 1, 1-2, 3-6, 11-16, and > 19 years and were 0.39 (± 0.1), 0.33 (± 0.1), 0.20 (± 0.02), 0.07 (± 0.02), and 0.05 (± 0.01) ng kg-1/day, respectively. Source apportionment estimate indicates PAHs bound in dust retained in ACU filters are originated from pyrogenic sources.

Human metabolic responses to chronic environmental polycyclic aromatic hydrocarbon exposure by a metabolomic approach.

The toxicities of polycyclic aromatic hydrocarbons (PAHs) have been extensively explored due to their carcinogenic and mutagenic potency; however, little is known about the metabolic responses to chronic environmental PAH exposure among the general population. In the present study, 566 healthy volunteers were dichotomized into exposed and control groups to investigate PAH-induced perturbations in the metabolic profiles. Nine urine PAH metabolites were measured by a sensitive LC-MS/MS method to comprehensively evaluate the PAH exposure level of each individual, and the metabolic profiles were characterized via a LC-MS-based metabolomic approach. PAH exposure was correlated to its metabolic outcomes by linear and logistic regression analyses. Metabolites related to amino acid, purine, lipid, and glucuronic acid metabolism were significantly changed in the exposed group. 1-Hydroxyphenanthrene and dodecadienylcarnitine have potential as sensitive and reliable biomarkers for PAH exposure and its metabolic outcomes, respectively, in the general population. These findings generally support the hypothesis that environmental PAH exposure causes oxidative stress-related effects in humans. The current study provides new insight into the early molecular events induced by PAH exposure in the actual environment.

Lung cancer risk from PAHs emitted from biomass combustion.

This study deals with the assessment of the cancer risk attributable to PAH exposure, attributable to the increased use of biomass for space heating in Greece in the winter of 2012-2013. Three fractions of particulates (PM1, PM2.5 and PM10) were measured in two sampling sites (urban/residential and traffic-influenced) followed by chemical analysis of 19 PAHs and levoglucosan (used as a biomarker tracer). PAH-induced lung cancer risk was estimated by a comprehensive methodology that incorporated human respiratory tract deposition modelling in order to estimate the toxic equivalent concentration (TEQ) at each target tissue. This allowed us to further differentiate internal exposure and risk by age groups. Results showed that all PM fractions are higher in Greece during the cold months of the year, mainly due to biomass use for space heating. PAH and levoglucosan levels were highly correlated, indicating that particles emitted from biomass combustion are more toxic than PM emitted from other sources. The estimated lung cancer risk was non-negligible for residents close to the urban background monitoring site. Higher risk was estimated for infants and children, due to the higher bodyweight normalized dose and the human respiratory tract (HRT) physiology. HRT structure and physiology in youngsters favor deposition of particles that are smaller and more toxic per unit mass. In all cases, the estimated risk (5.7E-07 and 1.4E-06 for the urban background site and 1.4E-07 to 5.0E-07 for the traffic site) was lower to the one estimated by the conventional methodology (2.8E-06 and 9.7E-07 for the urban background and the traffic site respectively) that is based on Inhalation Unit Risk; the latter assumes that all PAHs adsorbed on particles are taken up by humans. With the methodology proposed herein, the estimated risk presents a 5-7 times difference between the two sampling sites (depending on the age group). These differences could not have been identified had we relied only on conventional risk assessment method. Consequently, the actual cancer risk attributable to PAHs on PM emitted from biomass burning would have been significantly underestimated.

Vitamin D status in relation to inflammatory risk and albuminuria associated with polycyclic aromatic hydrocarbon exposure in the US population.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with both systematic inflammation and renal dysfunction. Reports have suggested that anti-inflammatory properties of vitamin D may provide protection against renal injury. This cross-sectional study tested the hypothesis that serum 25-hydroxyvitamin D [25(OH)D] moderates the inflammation and albuminuria associated with PAH exposure. Data were obtained from 5,982 subjects aged 20-79 years in the National Health and Nutrition Examination Survey (2001-2010). PAH exposure was estimated by urinary PAH metabolites. Inflammation was defined as serum C-reactive protein (CRP) > 3 mg/L and albuminuria as urinary albumin-to-creatinine ratio > 30 mg/g. The results found that greater PAH exposure was linked with inflammation and albuminuria. Individuals with PAH exposure also tended to have lower 25(OH)D and lower vitamin D was associated with both elevated CRP (Odds ratio [OR] = 1.28, 95% confidence interval [CI] = 1.07-1.54) and urinary albumin (1.35, 95%CI = 1.03-1.77) for any given PAH exposure. Those with lower serum 25(OH)D-to-urinary PAH ratios were likewise at a greater risk of elevated CRP and albuminuria. The findings support prior suggestions that exposure to PAHs is associated with inflammation and albuminuria but suggests further that the risk is higher when vitamin D is lower. Thus, nutritional status becomes an important variable in PAH risk assessment.

Relationship Between Polycyclic Aromatic Hydrocarbons and Cardiovascular Diseases: A Systematic Review.

Objective: The primary aim of this systematic review was to examine the relationship of polycyclic aromatic hydrocarbon (PAH) exposure with cardiovascular diseases (CVDs) and elaborate the current knowledge and recent advances in the area of PAH and its effects on CVDs and discuss the growing epidemiological evidence linking PAH to CVDs on the health of human populations. In this systematic review, the increased risk of cardiovascular diseases and their relationship with PAHs were discussed in detail. Methods: On 05th April 2021, a systematic literature search was conducted using PubMed/Medline and Web of Science search engines in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) criteria. The search was limited to articles that were written in English and dealt with human issues. All original peer-review publications were considered for inclusion. Comments, case reports, reviews, duplicated papers, and conference reports were excluded. Data was collected from included papers by two independent reviewers. Results: Conclusively, 20 research articles published between 2005 and 2021 were chosen for the final analysis. The systemic review included 20 studies with a variety of geographical studies. The most common research category among the nominated studies were time-series studies followed by retrospective cohort, cross-sectional, quasi-experimental, panel, and case-control studies. Most of the studies were conducted in the United States, whereas others were showed in various geographical countries around the world, such as Denmark, Germany, Finland, Netherlands, France, China, Norway, Korea, Sweden, Saudi Arabia, and Belgium. Eight studies assessed the association between PAH exposure and CVDs, four articles observed this relationship with blood pressure (BP), two observed association between atherosclerotic CVD and PAH, one congenital heart disease, cardiovascular events, and two with obesity. Furthermore, in some investigations, a favorable association between PAH exposure and hypertension as well as PAH exposure and obesity was found. Conclusion: In conclusion, this systematic review examined the relationship of PAH exposure with CVDs and CVD-related risk factors by searching several digital databases. After a comprehensive literature searches and summarizing findings from 20 articles, the authors concluded that a positive relationship was observed between PAH exposure and CVD risks.

Exposure and Absorption of PAHs in Wildland Firefighters: A Field Study with Pilot Interventions.

OBJECTIVES: There is limited knowledge of exposure to polycyclic aromatic hydrocarbons (PAHs) in wildland firefighters, or of the effectiveness of interventions to reduce this. This study of wildland firefighters assessed whether PAHs were present and considered respiratory protection and enhanced skin hygiene as possible interventions. METHODS: 1-Hydroxypyrene (1-HP) was measured in urine samples collected pre-shift, post-shift, and next morning from wildland firefighters in Alberta and British Columbia. Skin wipes, collected pre- and post-shift, were analysed for eight PAHs. Breathing zone air samples were analysed for 11 PAHs. As pilot interventions, participants were randomized to either normal or enhanced skin hygiene. A sample of volunteers was assigned to a disposable N95 mask or a half facepiece mask with P100 organic vapour cartridge. Participants completed a brief questionnaire on activities post-shift and respiratory symptoms. RESULTS: Non-smoking firefighters (66 male and 20 female) were recruited from 11 fire crews. Air sampling pumps were carried for the full shift by 28 firefighters, 25 firefighters wore masks (14 N95 and 11 P100); 42 were assigned to the enhanced skin hygiene intervention. Sixty had hot spotting as their main task. Air monitoring identified PAHs (benzo(b,j,k)fluoranthene in particulates, phenanthrene in the gaseous phase) for 6 of the 11 crews. PAHs (largely naphthalene) were found post-shift on 40/84 skin wipes from the hand and 38/84 from jaw/throat. The mean increase in 1-HP in urine samples collected after the shift (compared with samples collected before the shift) was 66 ng g-1 creatinine (P < 0.001) with an increase over the shift found for 76% of participants. 1-HP in next morning urine samples was significantly lower than at the end of shift (a reduction of 39.3 ng g-1: P < 0.001). The amount of naphthalene on skin wipes was greater at the end of the shift (post) than at the start (pre). The mean post-pre weight difference of naphthalene on skin wipes taken from the hand was 0.96 ng wipe-1 (P = 0.01) and from the jaw/throat 1.28 ng wipe-1 (P = 0.002). The enhanced skin hygiene intervention lead to a larger reduction in 1-HP between end of shift and next morning urine samples but only for those with naphthalene on skin wipes at the end of shift. The difference in 1-HP concentration in urine samples collected before and after the shift was reduced for those wearing a mask (linear tend P = 0.063, one-sided). In multivariable models, 1-HP at end of shift was related to gaseous phase phenanthrene, estimated from air sampling [ß = 318.2, 95% confidence interval (CI) 67.1-569.2]. Naphthalene on hand skin wipes reflected work in hot spotting during the shift (ß = 0.53, 95% CI 0.22-0.86). CONCLUSIONS: This study provided evidence of PAHs in the air and on the skin of many, but not all, fire crew. Absorbed PAHs, reflected in 1-HP in urine, increased over the shift. Results from the pilot interventions suggest that enhanced skin hygiene would reduce absorption post fire where PAHs had been accumulated on the skin, and that masks could be effective in reducing PAH inhalation exposure. Interventions to reduce PAH absorption are supported by the pilot work reported here and warrant further evaluation across a full fire season.

Association of internal exposure to polycyclic aromatic hydrocarbons with inflammation and oxidative stress in prediabetic and healthy individuals.

Polycyclic aromatic hydrocarbons (PAHs) are key air pollutants that may contribute to the risk of numerous diseases by inducing inflammation and oxidative stress. Individuals with metabolic disorders may be more susceptible to PAH-induced inflammation and oxidative stress. To test this hypothesis, we designed a panel study involving 60 patients with pre-type 2 diabetes (pre-T2D) and 60 reference participants, and conducted up to seven repeated clinical examinations. Urinary metabolites of PAHs (i.e., OH-PAHs), measured as indicators of total PAH exposure, showed significant associations with markers of respiratory and systemic inflammation, including exhaled nitric oxide, interleukin (IL)-6 in exhaled breath condensate, and blood IL-2 and IL-8 levels and leucocyte count. The most significant effect was on urinary malondiadehyde (MDA), a marker of lipid peroxidation; a onefold increase of OH-PAHs was associated with 9.2-46.0% elevation in MDA in pre-T2D participants and 9.8-31.2% increase in healthy references. Pre-T2D participants showed greater increase in MDA, suggesting that metabolic disorder enhanced the oxidative damage induced by PAH exposure. This study revealed the association between PAH exposure and markers of inflammation and oxidative stress, and the enhanced responses of pre-T2D patients suggested that individuals with metabolic disorders were more susceptible to the adverse health effects of PAH exposure.

Association between H3K36me3 modification and methylation of LINE-1 and MGMT in peripheral blood lymphocytes of PAH-exposed workers.

To explore the epigenetic alterations in response to DNA damage following polycyclic aromatic hydrocarbons (PAHs) exposure and the crosstalk between different epigenetic regulations, we examined trimethylated Lys 36 of histone H3 (H3K36me3) and methylation of 'long interspersed element-1 (LINE-1)' and 'O 6-methylguanine-DNA methyltransferase (MGMT)' in peripheral blood lymphocytes (PBLCs) of 173 coke oven workers (PAH-exposed group) and 94 non-exposed workers (control group). The PAH-exposed group showed higher internal PAH exposure level, enhanced DNA damage and increased MGMT expression (all P < 0.001). Notably, the methylation of LINE-1 and MGMT decreased by 3.9 and 40.8%, respectively, while H3K36me3 level was 1.7 times higher in PBLCs of PAH-exposed group compared to control group (all P < 0.001). These three epigenetic marks were significantly associated with DNA damage degree (all P < 0.001) and PAH exposure level in a dose-response manner (all P < 0.001). LINE-1 hypomethylation is correlated with enhanced H3K36me3 modification (ß = -0.198, P = 0.002), indicating a synergistic effect between histone modification and DNA methylation at the whole genome level. In addition, MGMT expression was positively correlated with H3K36me3 modification (r = 0.253, P < 0.001), but not negatively correlated with MGMT methylation (r = 0.202, P < 0.05). The in vitro study using human bronchial epithelial cells treated with the organic extract of coke oven emissions confirmed that H3K36me3 is important for MGMT expression following PAH exposure. In summary, our study indicates that histone modification and DNA methylation might have synergistic effects on DNA damage induced by PAH exposure at the whole genome level and H3K36me3 is more essential for MGMT expression during the course.

Ultra-high sensitive analysis of 3-hydroxybenzo[a]pyrene in human urine using GC-APLI-MS.

Urinary 3-hydroxybenzo[a]pyrene (3-OH-BaP) is a known biomarker for human exposure to carcinogenic polycyclic aromatic hydrocarbons (PAH). In this work, a new method for the ultra-sensitive quantification of this biomarker has been developed using the hyphenation of gas chromatography and atmospheric pressure laser ionization-mass spectrometry (GC-APLI-MS). In combination with an advanced sample preparation, a limit of detection (LOD) of 0.6 pg/L was achieved which is an improvement by a factor of at least 28 compared with existing methods. The limit of quantification (LOQ) is 1.8 pg/L. With this set-up 3-OH-BaP could be analyzed in urine samples of 7 smokers and 7 non-smokers. Concentrations ranged from 37 to 270 pg/L for non-smokers and from 374 to 1171 pg/L for smokers. For the first time, 3-OH-BaP was quantifiable in all non-smoker samples as no value was below the LOQ. Correlation of the urinary 3-OH-BaP values with the number of daily smoked cigarettes and with urinary cotinine values shows a clear relationship between 3-OH-BaP content and smoking habits. This innovative analytical method enables monitoring of low levels of the biomarker 3-OH-BaP in urine of non-occupationally exposed individuals including smokers, the general population with background PAH exposure and cohorts of low exposition such as newborns and children.

A multi-year study of hepatic biomarkers in coastal fishes from the Gulf of Mexico after the Deepwater Horizon Oil Spill.

Following the 2010 Gulf of Mexico oil spill, concerns were raised regarding exposure of fish to crude oil components, particularly polycyclic aromatic hydrocarbons (PAHs). This three year study examined hepatic enzymes in post-mitochondrial supernatant fractions from red snapper (Lutjanus campechanus) and gray triggerfish (Balistes capriscus) collected in the north central Gulf of Mexico between 2011 and 2014. Biomarker activities evaluated included benzo(a)pyrene hydroxylase (AHH), ethoxyresorufin O-deethylase (EROD), glutathione transferase (GST), and glutathione peroxidase (GPx). Mean EROD activity was higher in gray triggerfish (12.97 ± 7.15 pmol/min/mg protein [mean ± SD], n = 115) than red snapper (2.75 ± 1.92 pmol/min/mg protein, n = 194), p < 0.0001. In both species, EROD declined over time between 2011 and 2014. Declines in GST and GPx activities were also noted over this time period for both species. Gray triggerfish liver was fatty, and heptane extracts of the liver fat contained fluorescent substances with properties similar to known PAHs, however the origin of these PAHs is unknown.

Biomonitoring of polycyclic aromatic hydrocarbons exposure in small groups of residents in Brisbane, Australia and Hanoi, Vietnam, and those travelling between the two cities.

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been associated with adverse health outcomes. Concentrations of urinary PAH metabolites (OH-PAHs) provide an integrated measure of human exposure to PAHs but measurement of urinary OH-PAHs has not been done in Australia and rarely in Vietnam, where air pollution is of concern. In this study, we assessed exposure to PAHs in 16 participants living in Brisbane, Australia and Hanoi, Vietnam, with 4 participants travelling between the two cities during the monitoring period. A total of 312 first morning urine samples were collected over 10weeks and were analysed for nine OH-PAHs. Concentrations of the urinary OH-PAHs were 2-10 times higher in participants from Hanoi than those from Brisbane. For example, the median concentrations of 1-hydroxypyrene were 292pg/mL in Hanoi, compared to 64pg/mL in Brisbane. For participants travelling from Brisbane to Hanoi and back, differences in exposure to PAHs in these two cities resulted in corresponding changes of urinary OH-PAH concentrations, demonstrating that the more polluted environment in Hanoi was likely the source for higher PAH exposure there.

Antihistamine medication may alleviate negative effects of prenatal exposure to polycyclic aromatic hydrocarbons (PAH) on lung function in children. Birth cohort prospective study.

The main purpose of the present study was to test the hypothesis that the depressed lung growth attributable to prenatal exposure to polycyclic aromatic hydrocarbons (PAH) may be modified by the intake of antihistamine medications. Individual prenatal PAH exposure was assessed by personal air monitoring in 176 children who were followed over nine years, in the course of which outdoor residential air monitoring, allergic skin tests for indoor allergens, lung function tests (FVC, FEV(1), FEV(05), and FEF(25-75)) were performed. The analysis with the General Estimated Equation (GEE) showed no association between prenatal PAH exposure and lung function in the group of children who were reported to be antihistamine users. However, in the group of antihistamine non-users all lung function tests except for FEF(25-75) were significantly and inversely associated with prenatal airborne PAH exposure. The results of the study suggest that the intake of antihistamine medications in early childhood may inhibit the negative effect of fetal PAH exposure on lung growth and provides additional indirect evidence for the hypothesis that lung alterations in young children resulting from PAH exposure may be caused by the allergic inflammation within lung.

Separate and joint effects of tranplacental and postnatal inhalatory exposure to polycyclic aromatic hydrocarbons: prospective birth cohort study on wheezing events.

The goal of this epidemiologic investigation was to analyze the associations between prenatal and postnatal exposure to airborne polycyclic aromatic hydrocarbons (PAH) and severity of wheeze and recurrent wheeze. The 257 children included in this analysis had a complete set of prenatal and postnatal PAH measurements and attended regular health checkups over a 4-year follow-up period since birth. Transplacental PAH exposure was measured by personal air monitoring of the mothers during the second trimester of pregnancy; postnatal exposure was estimated using the same instruments indoors at the children's residences at age 3. Chemical analysis tests were performed to determine airborne concentrations of nine PAH compounds. The results show that both prenatal and postnatal exposure were associated positively with the severity of wheezing days and recurrent wheezing reported in the follow-up. While the incidence rate ratio (IRR) for severity of wheeze and prenatal PAH exposure was 1.53 (95%CI: 1.43-1.64) that for postnatal PAH exposure was 1.13 (95%CI: 1.08-1.19). However, recurrent wheezing was more strongly associated with airborne PAH levels measured at age 3 (OR = 2.31, 95%CI: 1.26-4.22) than transplacental PAH exposure (OR = 1.40, 95% CI: 0.85-2.09), but the difference was statistically insignificant. In conclusion, it appears that prenatal PAH exposure may precipitate and intensify early onset of wheezing symptoms in childhood, resulting from the postnatal exposure and suggest that success in reducing the incidence of respiratory diseases in children would depend on reducing both fetal and childhood exposure to air pollution.